NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment.
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
Here’s the problem.successfully translate DNA, but would sometimes tangle and die.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS. Look at it this way: before the evolution of topoisomerase, cells with DNA sequences approaching the threshold of requiring topoisomerase Untangle Assist [TM] would usually
Problem 1. That doesn’t leave NS anything to work with.
Problem 2. Irreducible complexity, it would appear? A partly evolved topoisomerase cannot untangle DNA and confer the selectable advantage described. Exaptation? If so, of what, and regardless, you still need an extended sequence of selectable steps toco-opt/adapt/build/tune that new and precise machine of 765 amino acids [1].
Problem 3. Multiple phenotypic traits would tend to overwhelm the blunt and binary selection action on any tentative steps in topoisomerase evolution.
A prediction of this analysis would be that evolution of core cellular machinery must have been largely complete very early on, and certainly before complex multicellular life, which would amplify Problem 3.
-----open and close in a precise order. It performs a series of steps that can best be described, based on the latest research, as follows:
[1] TOPOISOMERASE II OPERATION
Replication or transcription of DNA stresses the macromolecule, resulting in supercoiling. Topoisomerase II relieves the stress by reducing the number of supercoils. The enzyme is composed of two identical halves that combine to form three gates that
1. One DNA segment enters the upper gate and then binds to the middle gate. A second strand enters the top gate. The middle and lower gates are initially closed.
2. The middle gate cuts the first strand in two. Two ATP molecules attach to the upper gate, and the gate closes.
3. One of the ATP molecules breaks apart releasing energy that might help keep the upper gate together for the next steps.
4. The middle gate separates the two ends of the first DNA segment, creating a gap. Both DNA ends remain attached to the middle gate.
5. The second DNA segment moves through the gap.
6. The upper gate rotates. The middle gate closes, and the two DNA ends are reconnected.
7. The enzyme breaks apart the remaining ATP molecule, and the lower gate opens, allowing the second DNA segment to leave.
8. The lower gate closes, and the upper gate opens, releasing the first DNA segment.
After the last step, the topoisomerase is reset and ready to perform the same process again.
https://evolutionnews.org/2022/03/new-animation-on-topoisomerase-demonstrates-irrationality-of-denying-design-evidence-in-biology/
But "Selection" implies a decision, a consciousness. So people look for >logic, a linear progression... stupid stuff.
On Thursday, October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,
The above presses a gross misconception: that phenotype means "observable anatomical feature" . You compound this gross misunderstanding below.
Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation from which to debate the validity of the theory of evolution? Son, people can see you.
On Thursday, October 12, 2023 at 10:16:06 PM UTC+11, Lawyer Daggett wrote:incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Thursday, October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,
is part of the phenotype, insofar as it is a dynamic, chemically active, physical structure. It follows from this that the genotype is non-physical information, which is embodied in DNA.The above presses a gross misconception: that phenotype means "observable anatomical feature" . You compound this gross misunderstanding below.
Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation fromValid point - my premise should instead be stated something like this: "parts of the phenotype less accessible to natural selection". As regards the genotype/phenotype distinction, I would say that even the DNA itself (including protein coding regions)
which to debate the validity of the theory of evolution? Son, people can see you.
My question to you is, why the rage and vitriol?
On Thursday, October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,
successfully translate DNA, but would sometimes tangle and die.Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS. Look at it this way: before the evolution of topoisomerase, cells with DNA sequences approaching the threshold of requiring topoisomerase Untangle Assist [TM] would usually
problem" evolutionnews suggested to you applies to all genotypes and phenotypes. There are many steps between a gene sequence and the effect of that gene on an organism's fitness. All the genes are inside cells, as are, at least at first, all the geneProblem 1. That doesn’t leave NS anything to work with.Does topisomerase do anything useful for the organism? Sure seems like it. If that's the case, changes in topisomerase function would make the organism more fit or less fit, depending on the change - that's what natural selection acts on. And the "
to co-opt/adapt/build/tune that new and precise machine of 765 amino acids [1].Problem 2. Irreducible complexity, it would appear? A partly evolved topoisomerase cannot untangle DNA and confer the selectable advantage described. Exaptation? If so, of what, and regardless, you still need an extended sequence of selectable steps
Farther down in the post you list all the enzymatic activities that the topoisomerase complex carries out. Imagine a world in which nobody has a modern topoisomerase. In that world, could any of the many enzymatic activities listed below be useful?Could making a cut in a DNA strand be useful? Sure, lots of steps in replication, proof reading, etc require cutting (or joining) DNA strands. Could coupling the energy release from hydrolysis of ATP to mechanical twisting of DNA be useful for anything?
was a target of evolution and that selection on multiple phenotypic traits would push evolution away from that target. But that's pretty much backwards. Topoisomerase is where those genes just happened to end up as a result of all those complexProblem 3. Multiple phenotypic traits would tend to overwhelm the blunt and binary selection action on any tentative steps in topoisomerase evolution.Pretty hard to know what the guys at evolutionnews have in mind here. Almost all mutations have complex effects on phenotype, but I don't see why that prevents selection of different phenotypes. They seem to think (perhaps) that modern topoisomerase
better equip you to critique it. The folks at evolutionnews are not doing you any favors. They saw an animation of topoisomerase, a bright shiny object, and so they are all excited about it, but just about any enzyme or enzyme complex, membrane transportA prediction of this analysis would be that evolution of core cellular machinery must have been largely complete very early on, and certainly before complex multicellular life, which would amplify Problem 3.I think most would agree with evolutionnews that the evolution of core cellular machinery was largely complete before the evolution of complex multicellular life. I'm not sure why this would amplify the alleged Problem 3.
The fact that you could not think immediately of the reasons why problems 1 and 2 are not really problems (problem 3 seems so vague that I can't blame you for that) suggests that maybe you should read some basic textbook on evolution, even if only to
Biologists have noticed that cells are complex. For some reason, the overwhelming majority of them do not think that such complexity represents a devastating problem for the theory of evolution. It might be collective delusion and group think. It mightbe a desperate desire to hold on to the huge salaries and easy life style they have as adjunct assistant professors. It might a prior metaphysical commitment to a view of the world in which they won't be punished in eternity for doing drugs and cheating
open and close in a precise order. It performs a series of steps that can best be described, based on the latest research, as follows:-----
[1] TOPOISOMERASE II OPERATION
Replication or transcription of DNA stresses the macromolecule, resulting in supercoiling. Topoisomerase II relieves the stress by reducing the number of supercoils. The enzyme is composed of two identical halves that combine to form three gates that
1. One DNA segment enters the upper gate and then binds to the middle gate. A second strand enters the top gate. The middle and lower gates are initially closed.
2. The middle gate cuts the first strand in two. Two ATP molecules attach to the upper gate, and the gate closes.
3. One of the ATP molecules breaks apart releasing energy that might help keep the upper gate together for the next steps.
4. The middle gate separates the two ends of the first DNA segment, creating a gap. Both DNA ends remain attached to the middle gate.
5. The second DNA segment moves through the gap.
6. The upper gate rotates. The middle gate closes, and the two DNA ends are reconnected.
7. The enzyme breaks apart the remaining ATP molecule, and the lower gate opens, allowing the second DNA segment to leave.
8. The lower gate closes, and the upper gate opens, releasing the first DNA segment.
After the last step, the topoisomerase is reset and ready to perform the same process again.
https://evolutionnews.org/2022/03/new-animation-on-topoisomerase-demonstrates-irrationality-of-denying-design-evidence-in-biology/
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
Here’s the problem.successfully translate DNA, but would sometimes tangle and die.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS. Look at it this way: before the evolution of topoisomerase, cells with DNA sequences approaching the threshold of requiring topoisomerase Untangle Assist [TM] would usually
Problem 1. That doesn’t leave NS anything to work with.
Problem 2. Irreducible complexity, it would appear? A partly evolved topoisomerase cannot untangle DNA and confer the selectable advantage described. Exaptation? If so, of what, and regardless, you still need an extended sequence of selectable steps toco-opt/adapt/build/tune that new and precise machine of 765 amino acids [1].
Problem 3. Multiple phenotypic traits would tend to overwhelm the blunt and binary selection action on any tentative steps in topoisomerase evolution.
A prediction of this analysis would be that evolution of core cellular machinery must have been largely complete very early on, and certainly before complex multicellular life, which would amplify Problem 3.
-----open and close in a precise order. It performs a series of steps that can best be described, based on the latest research, as follows:
[1] TOPOISOMERASE II OPERATION
Replication or transcription of DNA stresses the macromolecule, resulting in supercoiling. Topoisomerase II relieves the stress by reducing the number of supercoils. The enzyme is composed of two identical halves that combine to form three gates that
1. One DNA segment enters the upper gate and then binds to the middle gate. A second strand enters the top gate. The middle and lower gates are initially closed.
2. The middle gate cuts the first strand in two. Two ATP molecules attach to the upper gate, and the gate closes.
3. One of the ATP molecules breaks apart releasing energy that might help keep the upper gate together for the next steps.
4. The middle gate separates the two ends of the first DNA segment, creating a gap. Both DNA ends remain attached to the middle gate.
5. The second DNA segment moves through the gap.
6. The upper gate rotates. The middle gate closes, and the two DNA ends are reconnected.
7. The enzyme breaks apart the remaining ATP molecule, and the lower gate opens, allowing the second DNA segment to leave.
8. The lower gate closes, and the upper gate opens, releasing the first DNA segment.
After the last step, the topoisomerase is reset and ready to perform the same process again.
https://evolutionnews.org/2022/03/new-animation-on-topoisomerase-demonstrates-irrationality-of-denying-design-evidence-in-biology/
On Thursday, October 12, 2023 at 10:46:06 PM UTC+11, broger...@gmail.com wrote:incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Thursday, October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,
successfully translate DNA, but would sometimes tangle and die.Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS. Look at it this way: before the evolution of topoisomerase, cells with DNA sequences approaching the threshold of requiring topoisomerase Untangle Assist [TM] would usually
problem" evolutionnews suggested to you applies to all genotypes and phenotypes. There are many steps between a gene sequence and the effect of that gene on an organism's fitness. All the genes are inside cells, as are, at least at first, all the geneProblem 1. That doesn’t leave NS anything to work with.Does topisomerase do anything useful for the organism? Sure seems like it. If that's the case, changes in topisomerase function would make the organism more fit or less fit, depending on the change - that's what natural selection acts on. And the "
On reflection, the DNA itself (including protein coding regions) is part of the phenotype, insofar as it is a dynamic, chemically active, physical structure (as are gene products, as you suggest). It follows from this that the genotype is non-physicalinformation, which is embodied in DNA.
"Does topoisomerase do anything useful for the organism?" Or more precisely, "Topoisomerase II precursors" (which may be other forms of topoisomerase). This is a key point of contention with IC, which I know has been done to death. My argument does notdepend on there being no potential precursors, but rather is questioning what is needed for "molecular macroevolution" (if I can use that term) or exaptation to form Topoisomerase II.
That is, even just largely co-opting pre-evolved components still requires precision integration, expansion, function tuning, etc. This would be a multistep process requiring positive selection pressure for each intermediate. Now, arguably this is notimpossible in principle: each intermediate might permit a slightly higher survival rate, but this seems very unlikely to be sustainable over the stepwise addition of whatever portion of the total 765 amino acids need to be discovered.
A related question here is, what minimum degree of gradualism is required for evolution to work? To what extent must the pathway fitness be monotonically increasing?
steps to co-opt/adapt/build/tune that new and precise machine of 765 amino acids [1].Problem 2. Irreducible complexity, it would appear? A partly evolved topoisomerase cannot untangle DNA and confer the selectable advantage described. Exaptation? If so, of what, and regardless, you still need an extended sequence of selectable
Could making a cut in a DNA strand be useful? Sure, lots of steps in replication, proof reading, etc require cutting (or joining) DNA strands. Could coupling the energy release from hydrolysis of ATP to mechanical twisting of DNA be useful for anything?Farther down in the post you list all the enzymatic activities that the topoisomerase complex carries out. Imagine a world in which nobody has a modern topoisomerase. In that world, could any of the many enzymatic activities listed below be useful?
Functional precursors would be better than none at all, granted. But see my comment above.was a target of evolution and that selection on multiple phenotypic traits would push evolution away from that target. But that's pretty much backwards. Topoisomerase is where those genes just happened to end up as a result of all those complex
Problem 3. Multiple phenotypic traits would tend to overwhelm the blunt and binary selection action on any tentative steps in topoisomerase evolution.Pretty hard to know what the guys at evolutionnews have in mind here. Almost all mutations have complex effects on phenotype, but I don't see why that prevents selection of different phenotypes. They seem to think (perhaps) that modern topoisomerase
better equip you to critique it. The folks at evolutionnews are not doing you any favors. They saw an animation of topoisomerase, a bright shiny object, and so they are all excited about it, but just about any enzyme or enzyme complex, membrane transportA prediction of this analysis would be that evolution of core cellular machinery must have been largely complete very early on, and certainly before complex multicellular life, which would amplify Problem 3.I think most would agree with evolutionnews that the evolution of core cellular machinery was largely complete before the evolution of complex multicellular life. I'm not sure why this would amplify the alleged Problem 3.
The fact that you could not think immediately of the reasons why problems 1 and 2 are not really problems (problem 3 seems so vague that I can't blame you for that) suggests that maybe you should read some basic textbook on evolution, even if only to
might be a desperate desire to hold on to the huge salaries and easy life style they have as adjunct assistant professors. It might a prior metaphysical commitment to a view of the world in which they won't be punished in eternity for doing drugs andBiologists have noticed that cells are complex. For some reason, the overwhelming majority of them do not think that such complexity represents a devastating problem for the theory of evolution. It might be collective delusion and group think. It
Well, that made me smile (at last a whistleblower on adjunct assistant professors), and I take your point. In the words of Mark Knopfler, "Two men say they're Jesus, one of them must be wrong.”evolution" will decrease and give way to wide recognition of major problems for the theory of evolution.
As I've said before, as we discover more and more about the complexity of cells and multicellular life, my prediction is the "overwhelming majority of them [who] do not think that such complexity represents a devastating problem for the theory of
that open and close in a precise order. It performs a series of steps that can best be described, based on the latest research, as follows:-----
[1] TOPOISOMERASE II OPERATION
Replication or transcription of DNA stresses the macromolecule, resulting in supercoiling. Topoisomerase II relieves the stress by reducing the number of supercoils. The enzyme is composed of two identical halves that combine to form three gates
1. One DNA segment enters the upper gate and then binds to the middle gate. A second strand enters the top gate. The middle and lower gates are initially closed.
2. The middle gate cuts the first strand in two. Two ATP molecules attach to the upper gate, and the gate closes.
3. One of the ATP molecules breaks apart releasing energy that might help keep the upper gate together for the next steps.
4. The middle gate separates the two ends of the first DNA segment, creating a gap. Both DNA ends remain attached to the middle gate.
5. The second DNA segment moves through the gap.
6. The upper gate rotates. The middle gate closes, and the two DNA ends are reconnected.
7. The enzyme breaks apart the remaining ATP molecule, and the lower gate opens, allowing the second DNA segment to leave.
8. The lower gate closes, and the upper gate opens, releasing the first DNA segment.
After the last step, the topoisomerase is reset and ready to perform the same process again.
https://evolutionnews.org/2022/03/new-animation-on-topoisomerase-demonstrates-irrationality-of-denying-design-evidence-in-biology/
On Thursday, October 12, 2023 at 10:16:06?PM UTC+11, Lawyer Daggett wrote:incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Thursday, October 12, 2023 at 6:06:06?AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,
The above presses a gross misconception: that phenotype means "observable >> anatomical feature" . You compound this gross misunderstanding below.
is part of the phenotype, insofar as it is a dynamic, chemically active, physical structure. It follows from this that the genotype is non-physical information, which is embodied in DNA.Here’s the problem.has any excuse for that misconception. It's grotesquely wrong.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS. >> I'm cutting you off. Nobody, who has completed even a high school biology course,
My question for you is, is that level of ignorance a proper foundation from >> which to debate the validity of the theory of evolution? Son, people can see you.
Valid point - my premise should instead be stated something like this: "parts of the phenotype less accessible to natural selection". As regards the genotype/phenotype distinction, I would say that even the DNA itself (including protein coding regions)
My question to you is, why the rage and vitriol?
On Thursday, October 12, 2023 at 10:16:06 PM UTC+11, Lawyer Daggett wrote:incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Thursday, October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,
.The above presses a gross misconception: that phenotype means "observable anatomical feature" . You compound this gross misunderstanding below.
Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation from
which to debate the validity of the theory of evolution? Son, people can see you.
Valid point - my premise should instead be stated something like this: "parts of the
phenotype less accessible to natural selection". As regards the genotype/phenotype
distinction, I would say that even the DNA itself (including protein coding regions)
is part of the phenotype, insofar as it is a dynamic, chemically active, physical
structure. It follows from this that the genotype is non-physical information,
which is embodied in DNA.
My question to you is, why the rage and vitriol?
On Fri, 13 Oct 2023 03:55:13 -0700 (PDT), MarkE <me22...@gmail.com>incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
wrote:
On Thursday, October 12, 2023 at 10:16:06?PM UTC+11, Lawyer Daggett wrote: >> On Thursday, October 12, 2023 at 6:06:06?AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,
From Oxford Languages:The above presses a gross misconception: that phenotype means "observable >> anatomical feature" . You compound this gross misunderstanding below.
"phenotype: the set of observable characteristics of an individual
resulting from the interaction of its genotype with the environment."
Not sure what Daggett's objection is here.
Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation from
which to debate the validity of the theory of evolution? Son, people can see you.
is part of the phenotype, insofar as it is a dynamic, chemically active, physical structure. It follows from this that the genotype is non-physical information, which is embodied in DNA.Valid point - my premise should instead be stated something like this: "parts of the phenotype less accessible to natural selection". As regards the genotype/phenotype distinction, I would say that even the DNA itself (including protein coding regions)
Stipulating for argument's sake that all you say above is technically correct, what's your point in saying it? It doesn't challenge natural selection. It doesn't support ID or Creationism. It's not an
especially significant biological fact.
My question to you is, why the rage and vitriol?Since you asked, here's my guess:
<https://www.youtube.com/watch?v=aME0qvhZ37o>
On Friday, October 13, 2023 at 6:56:06 AM UTC-4, MarkE wrote:incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Thursday, October 12, 2023 at 10:16:06 PM UTC+11, Lawyer Daggett wrote:
On Thursday, October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,
.
.The above presses a gross misconception: that phenotype means "observable
anatomical feature" . You compound this gross misunderstanding below.
Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation from
which to debate the validity of the theory of evolution? Son, people can see you.
Valid point - my premise should instead be stated something like this: "parts of the
phenotype less accessible to natural selection". As regards the genotype/phenotype
distinction, I would say that even the DNA itself (including protein coding regions)
is part of the phenotype, insofar as it is a dynamic, chemically active, physical
structure. It follows from this that the genotype is non-physical information,
which is embodied in DNA.
My question to you is, why the rage and vitriol?You're "correction" is still loaded is falsehoods. We're not talking about incorrect
deductions. We're talking about asserting false premises. It's bullshit.
It makes it evident that you have almost no understanding of even the terms "phenotype", "selections", and as such no understanding of evolution.
Imagine you are an auto mechanic, somebody drops off their car for repair and
you fix it. The car's computer had thrown some codes about about misfiring and
problems with certain voltage on some fuel injectors. You know your stuff so you strip off the plenum and get to the injectors, you take out your handy volt-ohm
meter and check the resistance across the indicated injector and it is a dead short.
You call up the customer and ask if they want you to go ahead and replace all of
the injectors while you are there as the car has over 90K miles and it will save
them a lot of money if you do them all now rather than have to do the tear down
again for one that will quite likely fail in the next 10-15K miles.
He gets upset and tells you you don't know what you're doing, you just need to
clear the computer code so you could pass your state inspection. It was a computer
problem, the engine was running fine. Sure, running fine with a fuel injector that
was shorted out.
The guy doesn't understand cars but he's telling you what the problem is.
The point is, you aren't seeing rage and vitriol. You are seeing exasperation.
You don't even understand a simple thing like selection and you are here evangelizing
about how evolution could not have produced X, Y, or Z.
Find an on-line course on population genetics. Take it. There will be math, and
lots of it. Not that you're ready for it, but you'll understand some of it. More significantly,
if you do it, you might begin to discover just how much you really don't know, and
something about the things you think you know that just ain't so.
On Friday, October 13, 2023 at 8:36:06 AM UTC-4, jillery wrote:gradual, incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Fri, 13 Oct 2023 03:55:13 -0700 (PDT), MarkE <me22...@gmail.com>
wrote:
On Thursday, October 12, 2023 at 10:16:06?PM UTC+11, Lawyer Daggett wrote:
On Thursday, October 12, 2023 at 6:06:06?AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the
The above presses a gross misconception: that phenotype means "observable
anatomical feature" . You compound this gross misunderstanding below. From Oxford Languages:
"phenotype: the set of observable characteristics of an individual resulting from the interaction of its genotype with the environment."
Not sure what Daggett's objection is here.That's a rotten definition, especially when you want to apply it scientifically.
It's rotten because so many will misunderstand "observable" to mean something
that you visually detect. If one has a more scientific notion of "observable" to
mean has a measurable effect, it's closer. A phenotype is a tangible consequence
of a genotype. It can be cryptic. A phenotype can produce improved resistance
to cold/heat, which won't be revealed outside of cold/hot conditions.
Regardless, it's clear MarkE was inclined to dismiss 'invisible' intracellular changes
as not being phenotype changes, which he thought couldn't be acted upon by natural selection.
regions) is part of the phenotype, insofar as it is a dynamic, chemically active, physical structure. It follows from this that the genotype is non-physical information, which is embodied in DNA.Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation from
which to debate the validity of the theory of evolution? Son, people can see you.
Valid point - my premise should instead be stated something like this: "parts of the phenotype less accessible to natural selection". As regards the genotype/phenotype distinction, I would say that even the DNA itself (including protein coding
Stipulating for argument's sake that all you say above is technically correct, what's your point in saying it? It doesn't challenge natural selection. It doesn't support ID or Creationism. It's not anIt's technically false, except where it isn't even false because it's gibberish.
especially significant biological fact.
My question to you is, why the rage and vitriol?Since you asked, here's my guess:
<https://www.youtube.com/watch?v=aME0qvhZ37o>As I used to have to say to my grandkids when they were little. Use your words.
On Friday, October 13, 2023 at 11:26:07 PM UTC+11, Lawyer Daggett wrote:gradual, incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Friday, October 13, 2023 at 6:56:06 AM UTC-4, MarkE wrote:
On Thursday, October 12, 2023 at 10:16:06 PM UTC+11, Lawyer Daggett wrote:
On Thursday, October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the
selection coefficients (i.e. assigning different probabilities to a range from lethal to neutral to slightly positive)..
.The above presses a gross misconception: that phenotype means "observable
anatomical feature" . You compound this gross misunderstanding below.
Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation from
which to debate the validity of the theory of evolution? Son, people can see you.
Valid point - my premise should instead be stated something like this: "parts of the
phenotype less accessible to natural selection". As regards the genotype/phenotype
distinction, I would say that even the DNA itself (including protein coding regions)
is part of the phenotype, insofar as it is a dynamic, chemically active, physical
structure. It follows from this that the genotype is non-physical information,
which is embodied in DNA.
My question to you is, why the rage and vitriol?You're "correction" is still loaded is falsehoods. We're not talking about incorrect
deductions. We're talking about asserting false premises. It's bullshit.
It makes it evident that you have almost no understanding of even the terms
"phenotype", "selections", and as such no understanding of evolution.
Imagine you are an auto mechanic, somebody drops off their car for repair and
you fix it. The car's computer had thrown some codes about about misfiring and
problems with certain voltage on some fuel injectors. You know your stuff so
you strip off the plenum and get to the injectors, you take out your handy volt-ohm
meter and check the resistance across the indicated injector and it is a dead short.
You call up the customer and ask if they want you to go ahead and replace all of
the injectors while you are there as the car has over 90K miles and it will save
them a lot of money if you do them all now rather than have to do the tear down
again for one that will quite likely fail in the next 10-15K miles.
He gets upset and tells you you don't know what you're doing, you just need to
clear the computer code so you could pass your state inspection. It was a computer
problem, the engine was running fine. Sure, running fine with a fuel injector that
was shorted out.
The guy doesn't understand cars but he's telling you what the problem is.
The point is, you aren't seeing rage and vitriol. You are seeing exasperation.
You don't even understand a simple thing like selection and you are here evangelizing
about how evolution could not have produced X, Y, or Z.
Find an on-line course on population genetics. Take it. There will be math, andPopulation genetics is mathematically difficult, and can be assisted by computer simulation. Out of curiosity I've previously written a program to explore population behaviour and allele fixation, using recombination and various profiles of mutation
lots of it. Not that you're ready for it, but you'll understand some of it. More significantly,
if you do it, you might begin to discover just how much you really don't know, and
something about the things you think you know that just ain't so.
Do you have different definitions of genotype and phenotype?
On Saturday, October 14, 2023 at 7:51:08 AM UTC-4, MarkE wrote:gradual, incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Friday, October 13, 2023 at 11:26:07 PM UTC+11, Lawyer Daggett wrote:
On Friday, October 13, 2023 at 6:56:06 AM UTC-4, MarkE wrote:
On Thursday, October 12, 2023 at 10:16:06 PM UTC+11, Lawyer Daggett wrote:
On Thursday, October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the
selection coefficients (i.e. assigning different probabilities to a range from lethal to neutral to slightly positive)..
.The above presses a gross misconception: that phenotype means "observable
anatomical feature" . You compound this gross misunderstanding below.
Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation from
which to debate the validity of the theory of evolution? Son, people can see you.
Valid point - my premise should instead be stated something like this: "parts of the
phenotype less accessible to natural selection". As regards the genotype/phenotype
distinction, I would say that even the DNA itself (including protein coding regions)
is part of the phenotype, insofar as it is a dynamic, chemically active, physical
structure. It follows from this that the genotype is non-physical information,
which is embodied in DNA.
My question to you is, why the rage and vitriol?You're "correction" is still loaded is falsehoods. We're not talking about incorrect
deductions. We're talking about asserting false premises. It's bullshit.
It makes it evident that you have almost no understanding of even the terms
"phenotype", "selections", and as such no understanding of evolution.
Imagine you are an auto mechanic, somebody drops off their car for repair and
you fix it. The car's computer had thrown some codes about about misfiring and
problems with certain voltage on some fuel injectors. You know your stuff so
you strip off the plenum and get to the injectors, you take out your handy volt-ohm
meter and check the resistance across the indicated injector and it is a dead short.
You call up the customer and ask if they want you to go ahead and replace all of
the injectors while you are there as the car has over 90K miles and it will save
them a lot of money if you do them all now rather than have to do the tear down
again for one that will quite likely fail in the next 10-15K miles.
He gets upset and tells you you don't know what you're doing, you just need to
clear the computer code so you could pass your state inspection. It was a computer
problem, the engine was running fine. Sure, running fine with a fuel injector that
was shorted out.
The guy doesn't understand cars but he's telling you what the problem is.
The point is, you aren't seeing rage and vitriol. You are seeing exasperation.
You don't even understand a simple thing like selection and you are here evangelizing
about how evolution could not have produced X, Y, or Z.
Find an on-line course on population genetics. Take it. There will be math, andPopulation genetics is mathematically difficult, and can be assisted by computer simulation. Out of curiosity I've previously written a program to explore population behaviour and allele fixation, using recombination and various profiles of mutation
lots of it. Not that you're ready for it, but you'll understand some of it. More significantly,
if you do it, you might begin to discover just how much you really don't know, and
something about the things you think you know that just ain't so.
cellular functions, like DNA replication, or transcription, or formation of chromatin, are somehow less accessible to natural selection than genes that effect things like body mass, or coloration, or beak shape. Any mutation that effects fitness in anyDo you have different definitions of genotype and phenotype?The problem with your claim that topoisomerase mutations are beyond the reach of natural selection has little to do with having an incorrect definition of phenotype or genotype. The problem is your idea that mutations that effect basic, internal
On Saturday, October 14, 2023 at 11:16:08 PM UTC+11, broger...@gmail.com wrote:gradual, incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Saturday, October 14, 2023 at 7:51:08 AM UTC-4, MarkE wrote:
On Friday, October 13, 2023 at 11:26:07 PM UTC+11, Lawyer Daggett wrote:
On Friday, October 13, 2023 at 6:56:06 AM UTC-4, MarkE wrote:
On Thursday, October 12, 2023 at 10:16:06 PM UTC+11, Lawyer Daggett wrote:
On Thursday, October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the
mutation selection coefficients (i.e. assigning different probabilities to a range from lethal to neutral to slightly positive)..
.The above presses a gross misconception: that phenotype means "observable
anatomical feature" . You compound this gross misunderstanding below.
Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation from
which to debate the validity of the theory of evolution? Son, people can see you.
Valid point - my premise should instead be stated something like this: "parts of the
phenotype less accessible to natural selection". As regards the genotype/phenotype
distinction, I would say that even the DNA itself (including protein coding regions)
is part of the phenotype, insofar as it is a dynamic, chemically active, physical
structure. It follows from this that the genotype is non-physical information,
which is embodied in DNA.
My question to you is, why the rage and vitriol?You're "correction" is still loaded is falsehoods. We're not talking about incorrect
deductions. We're talking about asserting false premises. It's bullshit.
It makes it evident that you have almost no understanding of even the terms
"phenotype", "selections", and as such no understanding of evolution.
Imagine you are an auto mechanic, somebody drops off their car for repair and
you fix it. The car's computer had thrown some codes about about misfiring and
problems with certain voltage on some fuel injectors. You know your stuff so
you strip off the plenum and get to the injectors, you take out your handy volt-ohm
meter and check the resistance across the indicated injector and it is a dead short.
You call up the customer and ask if they want you to go ahead and replace all of
the injectors while you are there as the car has over 90K miles and it will save
them a lot of money if you do them all now rather than have to do the tear down
again for one that will quite likely fail in the next 10-15K miles.
He gets upset and tells you you don't know what you're doing, you just need to
clear the computer code so you could pass your state inspection. It was a computer
problem, the engine was running fine. Sure, running fine with a fuel injector that
was shorted out.
The guy doesn't understand cars but he's telling you what the problem is.
The point is, you aren't seeing rage and vitriol. You are seeing exasperation.
You don't even understand a simple thing like selection and you are here evangelizing
about how evolution could not have produced X, Y, or Z.
Find an on-line course on population genetics. Take it. There will be math, andPopulation genetics is mathematically difficult, and can be assisted by computer simulation. Out of curiosity I've previously written a program to explore population behaviour and allele fixation, using recombination and various profiles of
lots of it. Not that you're ready for it, but you'll understand some of it. More significantly,
if you do it, you might begin to discover just how much you really don't know, and
something about the things you think you know that just ain't so.
cellular functions, like DNA replication, or transcription, or formation of chromatin, are somehow less accessible to natural selection than genes that effect things like body mass, or coloration, or beak shape. Any mutation that effects fitness in anyDo you have different definitions of genotype and phenotype?The problem with your claim that topoisomerase mutations are beyond the reach of natural selection has little to do with having an incorrect definition of phenotype or genotype. The problem is your idea that mutations that effect basic, internal
To repeat an example: the development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.steps with positive selection pressure applied.
The evolution of Topoisomerase II may include some functional intermediates or it may co-opt extant subcomponents, but either way, its high informational and functional specificity and complexity will similarly necessitate gradual refinement over many
The evolutionary pathway of an eye can be conceived of as a long series of small variations each producing *functional* intermediates. But this is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-functional*in terms of *progression towards Topoisomerase II function*. That's the problem.
On Saturday, October 14, 2023 at 8:26:07 AM UTC-4, MarkE wrote:
On Saturday, October 14, 2023 at 11:16:08 PM UTC+11,Why do you think intermediates will be non-functional, even in terms of progression to topoisomerase II function? That function requires
broger...@gmail.com wrote:> > On Saturday, October 14, 2023 at 7:51:08
AM UTC-4, MarkE wrote:> > > On Friday, October 13, 2023 at 11:26:07 PM
UTC+11, Lawyer Daggett wrote:> > > > On Friday, October 13, 2023 at
6:56:06 AM UTC-4, MarkE wrote:> > > > > On Thursday, October 12, 2023
at 10:16:06 PM UTC+11, Lawyer Daggett wrote:> > > > > > On Thursday,
October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:> > > > > > > NS acts
on the phenotype, selecting on the basis of its traits or behaviours in
a given environment. For example, Galapagos finches beak size selected
as a result of the varying availability of large hard seeds or small
soft seeds. Or the gradual, incremental development of the camera-style
eyes of vertebrates. In both examples, NS has direct “visibility” of
the competing variants.> > > > .> > > > > > The above presses a gross
misconception: that phenotype means "observable> > > > > > anatomical
feature" . You compound this gross misunderstanding below.> > > > .> >
topoisomerase, for example, contains 765 amino acids. Topoisomerase IIHere’s the problem.> > > > > > >> > > > > > > Human
gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it
has very high information content (765 units) and functional complexity
and specificity.> > > > > > >> > > > > > > But this is all happening
inside the cell, out of the direct reach of NS.> > > > > > I'm cutting
you off. Nobody, who has completed even a high school biology course,>
wrong.> > > > > >> > > > > > My question for you is, is that level ofhas any excuse for that misconception. It's grotesquely
ignorance a proper foundation from> > > > > > which to debate the
validity of the theory of evolution? Son, people can see you.> > > >> >
this: "parts of the> > > > > phenotype less accessible to naturalValid point - my premise should instead be stated something like
selection". As regards the genotype/phenotype> > > > > distinction, I
would say that even the DNA itself (including protein coding regions)>
chemically active, physical> > > > > structure. It follows from thisis part of the phenotype, insofar as it is a dynamic,
that the genotype is non-physical information,> > > > > which is
embodied in DNA.> > > > >> > > > > My question to you is, why the rage
and vitriol?> > > > You're "correction" is still loaded is falsehoods.
We're not talking about incorrect> > > > deductions. We're talking
about asserting false premises. It's bullshit.> > > >> > > > It makes
it evident that you have almost no understanding of even the terms> > >
"phenotype", "selections", and as such no understanding ofevolution.> > > >> > > > Imagine you are an auto mechanic, somebody
drops off their car for repair and> > > > you fix it. The car's
computer had thrown some codes about about misfiring and> > > >
problems with certain voltage on some fuel injectors. You know your
stuff so> > > > you strip off the plenum and get to the injectors, you
take out your handy volt-ohm> > > > meter and check the resistance
across the indicated injector and it is a dead short.> > > >> > > > You
call up the customer and ask if they want you to go ahead and replace
all of> > > >> > > > the injectors while you are there as the car has
over 90K miles and it will save> > > > them a lot of money if you do
them all now rather than have to do the tear down> > > > again for one
that will quite likely fail in the next 10-15K miles.> > > >> > > > He
gets upset and tells you you don't know what you're doing, you just
need to> > > > clear the computer code so you could pass your state
inspection. It was a computer> > > > problem, the engine was running
fine. Sure, running fine with a fuel injector that> > > > was shorted
out.> > > >> > > > The guy doesn't understand cars but he's telling you
what the problem is.> > > >> > > > The point is, you aren't seeing rage
and vitriol. You are seeing exasperation.> > > > You don't even
understand a simple thing like selection and you are here evangelizing>
be math, and> > > > lots of it. Not that you're ready for it, butabout how evolution could not have produced X, Y, or Z.> > > >> >Find an on-line course on population genetics. Take it. There will
you'll understand some of it. More significantly,> > > > if you do it,
you might begin to discover just how much you really don't know, and> >
assisted by computer simulation. Out of curiosity I've previouslysomething about the things you think you know that just ain't so.>
Population genetics is mathematically difficult, and can be
written a program to explore population behaviour and allele fixation,
using recombination and various profiles of mutation selection
coefficients (i.e. assigning different probabilities to a range from
lethal to neutral to slightly positive).> > >> > > Do you have
different definitions of genotype and phenotype?> > The problem with
your claim that topoisomerase mutations are beyond the reach of natural
selection has little to do with having an incorrect definition of
phenotype or genotype. The problem is your idea that mutations that
effect basic, internal cellular functions, like DNA replication, or
transcription, or formation of chromatin, are somehow less accessible
to natural selection than genes that effect things like body mass, or
coloration, or beak shape. Any mutation that effects fitness in any
way, no matter where that effect occurs in the organism, is accessible
to natural selection. And no matter where in the organism the effect
occurs, there is always a long chain of effects between the mutation
itself and whatever effect it has on fitness. There is nothing special
in that regard about mutations in topoisomerase genes.
To repeat an example: the development of the camera-style eyes of
vertebrates requires gradual refinement over many steps with positive
selection pressure applied.>> The evolution of Topoisomerase II may
include some functional intermediates or it may co-opt extant
subcomponents, but either way, its high informational and functional
specificity and complexity will similarly necessitate gradual
refinement over many steps with positive selection pressure applied.>>
The evolutionary pathway of an eye can be conceived of as a long series
of small variations each producing *functional* intermediates. But this
is much more difficult with the evolution of Topoisomerase II. Most
intermediates will be *non-functional* in terms of *progression towards
Topoisomerase II function*. That's the problem.
various enzymatic activities, various specific bindings. Why can't
changes in the amino acid sequence (and hence the 3-d structure) lead
to slightly better substrate binding, slightly increased enzymatic
activity, etc? How is this different than gradual refinement of any biological activity?
On 2023-10-14 13:04:27 +0000, broger...@gmail.com said:
On Saturday, October 14, 2023 at 8:26:07 AM UTC-4, MarkE wrote:The problem is that MarkE knows no biochemistry, and just repeats stuff
On Saturday, October 14, 2023 at 11:16:08 PM UTC+11,Why do you think intermediates will be non-functional, even in terms of progression to topoisomerase II function? That function requires
broger...@gmail.com wrote:> > On Saturday, October 14, 2023 at 7:51:08
AM UTC-4, MarkE wrote:> > > On Friday, October 13, 2023 at 11:26:07 PM >> UTC+11, Lawyer Daggett wrote:> > > > On Friday, October 13, 2023 at
6:56:06 AM UTC-4, MarkE wrote:> > > > > On Thursday, October 12, 2023 >> at 10:16:06 PM UTC+11, Lawyer Daggett wrote:> > > > > > On Thursday,
October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:> > > > > > > NS acts >> on the phenotype, selecting on the basis of its traits or behaviours in >> a given environment. For example, Galapagos finches beak size selected
as a result of the varying availability of large hard seeds or small
soft seeds. Or the gradual, incremental development of the camera-style >> eyes of vertebrates. In both examples, NS has direct “visibility” of >> the competing variants.> > > > .> > > > > > The above presses a gross
misconception: that phenotype means "observable> > > > > > anatomical
feature" . You compound this gross misunderstanding below.> > > > .> >
topoisomerase, for example, contains 765 amino acids. Topoisomerase IIHere’s the problem.> > > > > > >> > > > > > > Human
gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it >> has very high information content (765 units) and functional complexity >> and specificity.> > > > > > >> > > > > > > But this is all happening
inside the cell, out of the direct reach of NS.> > > > > > I'm cutting
you off. Nobody, who has completed even a high school biology course,>
wrong.> > > > > >> > > > > > My question for you is, is that level ofhas any excuse for that misconception. It's grotesquely
ignorance a proper foundation from> > > > > > which to debate the
validity of the theory of evolution? Son, people can see you.> > > >> > >> > > > Valid point - my premise should instead be stated something like
this: "parts of the> > > > > phenotype less accessible to natural
selection". As regards the genotype/phenotype> > > > > distinction, I
would say that even the DNA itself (including protein coding regions)>
chemically active, physical> > > > > structure. It follows from thisis part of the phenotype, insofar as it is a dynamic,
that the genotype is non-physical information,> > > > > which is
embodied in DNA.> > > > >> > > > > My question to you is, why the rage
and vitriol?> > > > You're "correction" is still loaded is falsehoods.
We're not talking about incorrect> > > > deductions. We're talking
about asserting false premises. It's bullshit.> > > >> > > > It makes
it evident that you have almost no understanding of even the terms> > > >> > "phenotype", "selections", and as such no understanding of
evolution.> > > >> > > > Imagine you are an auto mechanic, somebody
drops off their car for repair and> > > > you fix it. The car's
computer had thrown some codes about about misfiring and> > > >
problems with certain voltage on some fuel injectors. You know your
stuff so> > > > you strip off the plenum and get to the injectors, you
take out your handy volt-ohm> > > > meter and check the resistance
across the indicated injector and it is a dead short.> > > >> > > > You >> call up the customer and ask if they want you to go ahead and replace
all of> > > >> > > > the injectors while you are there as the car has
over 90K miles and it will save> > > > them a lot of money if you do
them all now rather than have to do the tear down> > > > again for one
that will quite likely fail in the next 10-15K miles.> > > >> > > > He
gets upset and tells you you don't know what you're doing, you just
need to> > > > clear the computer code so you could pass your state
inspection. It was a computer> > > > problem, the engine was running
fine. Sure, running fine with a fuel injector that> > > > was shorted
out.> > > >> > > > The guy doesn't understand cars but he's telling you >> what the problem is.> > > >> > > > The point is, you aren't seeing rage >> and vitriol. You are seeing exasperation.> > > > You don't even
understand a simple thing like selection and you are here evangelizing> >> > > > about how evolution could not have produced X, Y, or Z.> > > >> > >> > > Find an on-line course on population genetics. Take it. There will
be math, and> > > > lots of it. Not that you're ready for it, but
you'll understand some of it. More significantly,> > > > if you do it,
you might begin to discover just how much you really don't know, and> > >> > > something about the things you think you know that just ain't so.>
assisted by computer simulation. Out of curiosity I've previouslyPopulation genetics is mathematically difficult, and can be
written a program to explore population behaviour and allele fixation,
using recombination and various profiles of mutation selection
coefficients (i.e. assigning different probabilities to a range from
lethal to neutral to slightly positive).> > >> > > Do you have
different definitions of genotype and phenotype?> > The problem with
your claim that topoisomerase mutations are beyond the reach of natural >> selection has little to do with having an incorrect definition of
phenotype or genotype. The problem is your idea that mutations that
effect basic, internal cellular functions, like DNA replication, or
transcription, or formation of chromatin, are somehow less accessible
to natural selection than genes that effect things like body mass, or
coloration, or beak shape. Any mutation that effects fitness in any
way, no matter where that effect occurs in the organism, is accessible
to natural selection. And no matter where in the organism the effect
occurs, there is always a long chain of effects between the mutation
itself and whatever effect it has on fitness. There is nothing special
in that regard about mutations in topoisomerase genes.
To repeat an example: the development of the camera-style eyes of
vertebrates requires gradual refinement over many steps with positive
selection pressure applied.>> The evolution of Topoisomerase II may
include some functional intermediates or it may co-opt extant
subcomponents, but either way, its high informational and functional
specificity and complexity will similarly necessitate gradual
refinement over many steps with positive selection pressure applied.>>
The evolutionary pathway of an eye can be conceived of as a long series >> of small variations each producing *functional* intermediates. But this >> is much more difficult with the evolution of Topoisomerase II. Most
intermediates will be *non-functional* in terms of *progression towards >> Topoisomerase II function*. That's the problem.
various enzymatic activities, various specific bindings. Why can't
changes in the amino acid sequence (and hence the 3-d structure) lead
to slightly better substrate binding, slightly increased enzymatic activity, etc? How is this different than gradual refinement of any biological activity?
he's found in creationist publications. It's probably a waste of time arfuing with him. So far the specific point is concerned we *know* from Steve Benner's work (on ribonuclease, for example) that the catalytic activity of ancestral forms can be measured.
--
athel cb : Biochemical Evolution, Garland Science, 2016
Not so. I accepted the correction that these are indeed phenotype
changes (e.g. lactose metabolism in bacteria). But my argument is that substantial intracellular changes (what might be called "molecular macroevolution") may be less accessible to NS. For example, the
development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.
The
evolution of Topoisomerase II may include some functional intermediates
or it may co-opt extant subcomponents, but either way, its informational
and functional specificity and complexity will similarly necessitate
gradual refinement over many steps with positive selection pressure
applied.
The development pathway of an eye can be conceived as long
series of small variations each producing *functional* intermediates.
This is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-functional* in terms of progression towards Topoisomerase II function. That's the problem.
On 14/10/2023 13:15, MarkE wrote:
Not so. I accepted the correction that these are indeed phenotype
changes (e.g. lactose metabolism in bacteria). But my argument is that substantial intracellular changes (what might be called "molecular macroevolution") may be less accessible to NS. For example, the development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.
The
evolution of Topoisomerase II may include some functional intermediates
or it may co-opt extant subcomponents, but either way, its informational and functional specificity and complexity will similarly necessitate gradual refinement over many steps with positive selection pressure applied.
The development pathway of an eye can be conceived as longThat's not what you seemed to be claiming before. You were claiming that
series of small variations each producing *functional* intermediates.
This is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-functional* in terms of progression towards Topoisomerase II function. That's the problem.
it wasn't accessible to natural selection. You're now claiming an
absence of functional intermediates, which is not the same thing. "Accessible to natural selection" and "accessible by natural selection"
may be only a small change in sequence, but it's a large change in semantics.
Anyway, creationists have long claimed that eyes are unevolvable due to
a putative lack of intermediates. Why should we take your claim about topoisomerases more seriously that their claims about eyes? Picking a
darker crevice (topoisomerases evolved longer ago, so more of the
evidence has been erased by time) for your gap doesn't make the argument better.
--
alias Ernest Major
On Sunday, October 15, 2023 at 12:21:08 AM UTC+11, Athel Cornish-Bowden wrote:coherent and substantive critique of my proposition. Rather, you offer a lazy "Steve Benner said..."
On 2023-10-14 13:04:27 +0000, broger...@gmail.com said:
Actually, I think your problem is you really don't like anyone challenging the naturalist position. I've noticed your own tactic is either to not respond, or make unsubstantiated dismissive remarks like this one. What is conspicuously missing is aOn Saturday, October 14, 2023 at 8:26:07 AM UTC-4, MarkE wrote:The problem is that MarkE knows no biochemistry, and just repeats stuff he's found in creationist publications. It's probably a waste of time arfuing with him. So far the specific point is concerned we *know* from Steve Benner's work (on ribonuclease, for example) that the catalytic activity of ancestral forms can be measured.
On Saturday, October 14, 2023 at 11:16:08 PM UTC+11,Why do you think intermediates will be non-functional, even in terms of progression to topoisomerase II function? That function requires
broger...@gmail.com wrote:> > On Saturday, October 14, 2023 at 7:51:08 >> AM UTC-4, MarkE wrote:> > > On Friday, October 13, 2023 at 11:26:07 PM
UTC+11, Lawyer Daggett wrote:> > > > On Friday, October 13, 2023 at
6:56:06 AM UTC-4, MarkE wrote:> > > > > On Thursday, October 12, 2023 >> at 10:16:06 PM UTC+11, Lawyer Daggett wrote:> > > > > > On Thursday, >> October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:> > > > > > > NS acts
on the phenotype, selecting on the basis of its traits or behaviours in >> a given environment. For example, Galapagos finches beak size selected >> as a result of the varying availability of large hard seeds or small
soft seeds. Or the gradual, incremental development of the camera-style >> eyes of vertebrates. In both examples, NS has direct “visibility” of
the competing variants.> > > > .> > > > > > The above presses a gross >> misconception: that phenotype means "observable> > > > > > anatomical >> feature" . You compound this gross misunderstanding below.> > > > .> > >> > > > > > Here’s the problem.> > > > > > >> > > > > > > Human
topoisomerase, for example, contains 765 amino acids. Topoisomerase II >> gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it >> has very high information content (765 units) and functional complexity >> and specificity.> > > > > > >> > > > > > > But this is all happening
inside the cell, out of the direct reach of NS.> > > > > > I'm cutting >> you off. Nobody, who has completed even a high school biology course,> >> > > > > > has any excuse for that misconception. It's grotesquely
wrong.> > > > > >> > > > > > My question for you is, is that level of >> ignorance a proper foundation from> > > > > > which to debate the
validity of the theory of evolution? Son, people can see you.> > > >> > >> > > > Valid point - my premise should instead be stated something like >> this: "parts of the> > > > > phenotype less accessible to natural
selection". As regards the genotype/phenotype> > > > > distinction, I >> would say that even the DNA itself (including protein coding regions)> >> > > > > is part of the phenotype, insofar as it is a dynamic,
chemically active, physical> > > > > structure. It follows from this
that the genotype is non-physical information,> > > > > which is
embodied in DNA.> > > > >> > > > > My question to you is, why the rage >> and vitriol?> > > > You're "correction" is still loaded is falsehoods. >> We're not talking about incorrect> > > > deductions. We're talking
about asserting false premises. It's bullshit.> > > >> > > > It makes >> it evident that you have almost no understanding of even the terms> > > >> > "phenotype", "selections", and as such no understanding of
evolution.> > > >> > > > Imagine you are an auto mechanic, somebody
drops off their car for repair and> > > > you fix it. The car's
computer had thrown some codes about about misfiring and> > > >
problems with certain voltage on some fuel injectors. You know your
stuff so> > > > you strip off the plenum and get to the injectors, you >> take out your handy volt-ohm> > > > meter and check the resistance
across the indicated injector and it is a dead short.> > > >> > > > You >> call up the customer and ask if they want you to go ahead and replace >> all of> > > >> > > > the injectors while you are there as the car has >> over 90K miles and it will save> > > > them a lot of money if you do
them all now rather than have to do the tear down> > > > again for one >> that will quite likely fail in the next 10-15K miles.> > > >> > > > He >> gets upset and tells you you don't know what you're doing, you just
need to> > > > clear the computer code so you could pass your state
inspection. It was a computer> > > > problem, the engine was running
fine. Sure, running fine with a fuel injector that> > > > was shorted >> out.> > > >> > > > The guy doesn't understand cars but he's telling you >> what the problem is.> > > >> > > > The point is, you aren't seeing rage >> and vitriol. You are seeing exasperation.> > > > You don't even
understand a simple thing like selection and you are here evangelizing> >> > > > about how evolution could not have produced X, Y, or Z.> > > >> > >> > > Find an on-line course on population genetics. Take it. There will >> be math, and> > > > lots of it. Not that you're ready for it, but
you'll understand some of it. More significantly,> > > > if you do it, >> you might begin to discover just how much you really don't know, and> > >> > > something about the things you think you know that just ain't so.> >> > > Population genetics is mathematically difficult, and can be
assisted by computer simulation. Out of curiosity I've previously
written a program to explore population behaviour and allele fixation, >> using recombination and various profiles of mutation selection
coefficients (i.e. assigning different probabilities to a range from
lethal to neutral to slightly positive).> > >> > > Do you have
different definitions of genotype and phenotype?> > The problem with
your claim that topoisomerase mutations are beyond the reach of natural >> selection has little to do with having an incorrect definition of
phenotype or genotype. The problem is your idea that mutations that
effect basic, internal cellular functions, like DNA replication, or
transcription, or formation of chromatin, are somehow less accessible >> to natural selection than genes that effect things like body mass, or >> coloration, or beak shape. Any mutation that effects fitness in any
way, no matter where that effect occurs in the organism, is accessible >> to natural selection. And no matter where in the organism the effect
occurs, there is always a long chain of effects between the mutation
itself and whatever effect it has on fitness. There is nothing special >> in that regard about mutations in topoisomerase genes.
To repeat an example: the development of the camera-style eyes of
vertebrates requires gradual refinement over many steps with positive >> selection pressure applied.>> The evolution of Topoisomerase II may
include some functional intermediates or it may co-opt extant
subcomponents, but either way, its high informational and functional
specificity and complexity will similarly necessitate gradual
refinement over many steps with positive selection pressure applied.>> >> The evolutionary pathway of an eye can be conceived of as a long series >> of small variations each producing *functional* intermediates. But this >> is much more difficult with the evolution of Topoisomerase II. Most
intermediates will be *non-functional* in terms of *progression towards >> Topoisomerase II function*. That's the problem.
various enzymatic activities, various specific bindings. Why can't changes in the amino acid sequence (and hence the 3-d structure) lead
to slightly better substrate binding, slightly increased enzymatic activity, etc? How is this different than gradual refinement of any biological activity?
Once more: the development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.steps with positive selection pressure applied.
The evolution of Topoisomerase II may include some functional intermediates or it may co-opt extant subcomponents, but either way, its high informational and functional specificity and complexity will similarly necessitate gradual refinement over many
The evolutionary pathway of an eye can be conceived of as a long series of small variations each producing *functional* intermediates. But this is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-functional*in terms of *progression towards Topoisomerase II function*. Regardless of Steve Benner's work (on ribonuclease, for example).
That's the problem.
--
athel cb : Biochemical Evolution, Garland Science, 2016
On Saturday, October 14, 2023 at 9:56:08 AM UTC-4, MarkE wrote:
On Sunday, October 15, 2023 at 12:21:08 AM UTC+11, Athel
Cornish-Bowden wrote:> > On 2023-10-14 13:04:27 +0000,
broger...@gmail.com said:> >> > > On Saturday, October 14, 2023 at
8:26:07 AM UTC-4, MarkE wrote:> > >> On Saturday, October 14, 2023 at
11:16:08 PM UTC+11,> > >> broger...@gmail.com wrote:> > On Saturday,
October 14, 2023 at 7:51:08> > >> AM UTC-4, MarkE wrote:> > > On
Friday, October 13, 2023 at 11:26:07 PM> > >> UTC+11, Lawyer Daggett
wrote:> > > > On Friday, October 13, 2023 at> > >> 6:56:06 AM UTC-4,
MarkE wrote:> > > > > On Thursday, October 12, 2023> > >> at
10:16:06 PM UTC+11, Lawyer Daggett wrote:> > > > > > On Thursday,> >
acts> > >> on the phenotype, selecting on the basis of its traits orOctober 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:> > > > > > > NS
behaviours in> > >> a given environment. For example, Galapagos finches
beak size selected> > >> as a result of the varying availability of
large hard seeds or small> > >> soft seeds. Or the gradual, incremental
development of the camera-style> > >> eyes of vertebrates. In both
examples, NS has direct “visibility” of> > >> the competing
variants.> > > > .> > > > > > The above presses a gross> > >>
misconception: that phenotype means "observable> > > > > > anatomical>
Human> > >> topoisomerase, for example, contains 765 amino acids.feature" . You compound this gross misunderstanding below.> > > >
Here’s the problem.> > > > > > >> > > > > > >
Topoisomerase II> > >> gathers, clamps, snips, swaps, and rejoins DNA
strands [1]. That is, it> > >> has very high information content (765
units) and functional complexity> > >> and specificity.> > > > > > >> >
direct reach of NS.> > > > > > I'm cutting> > >> you off. Nobody, whoBut this is all happening> > >> inside the cell, out of the
has completed even a high school biology course,>> > >> > > > > > has
any excuse for that misconception. It's grotesquely> > >> wrong.> > > >
a proper foundation from> > > > > > which to debate the> > >> validityMy question for you is, is that level of> > >> ignorance
of the theory of evolution? Son, people can see you.> > > >> >> > >> >
regions)>> > >> > > > > is part of the phenotype, insofar as it is aValid point - my premise should instead be stated something like> >
this: "parts of the> > > > > phenotype less accessible to natural> >
selection". As regards the genotype/phenotype> > > > > distinction,
would say that even the DNA itself (including protein coding
dynamic,> > >> chemically active, physical> > > > > structure. It
follows from this> > >> that the genotype is non-physical information,>
to you is, why the rage> > >> and vitriol?> > > > You're "correction"which is> > >> embodied in DNA.> > > > >> > > > > My question
is still loaded is falsehoods.> > >> We're not talking about incorrect>
It's bullshit.> > > >> > > > It makes> > >> it evident that you havedeductions. We're talking> > >> about asserting false premises.
almost no understanding of even the terms> > >> > >> > "phenotype",
"selections", and as such no understanding of> > >> evolution.> > > >>
car for repair and> > > > you fix it. The car's> > >> computer hadImagine you are an auto mechanic, somebody> > >> drops off their
thrown some codes about about misfiring and> > > >> > >> problems with
certain voltage on some fuel injectors. You know your> > >> stuff so> >
out your handy volt-ohm> > > > meter and check the resistance> > >>you strip off the plenum and get to the injectors, you> > >> take
across the indicated injector and it is a dead short.> > > >> > > >
replace> > >> all of> > > >> > > > the injectors while you are there ascall up the customer and ask if they want you to go ahead and
the car has> > >> over 90K miles and it will save> > > > them a lot of
money if you do> > >> them all now rather than have to do the tear
down> > > > again for one> > >> that will quite likely fail in the next
10-15K miles.> > > >> > > > He> > >> gets upset and tells you you don't
know what you're doing, you just> > >> need to> > > > clear the
computer code so you could pass your state> > >> inspection. It was a
computer> > > > problem, the engine was running> > >> fine. Sure,
running fine with a fuel injector that> > > > was shorted> > >> out.> >
what the problem is.> > > >> > > > The point is, you aren't seeingThe guy doesn't understand cars but he's telling you> > >>
rage> > >> and vitriol. You are seeing exasperation.> > > > You don't
even> > >> understand a simple thing like selection and you are here
evangelizing>> > >> > > > about how evolution could not have produced
X, Y, or Z.> > > >> >> > >> > > Find an on-line course on population
genetics. Take it. There will> > >> be math, and> > > > lots of it. Not
that you're ready for it, but> > >> you'll understand some of it. More
significantly,> > > > if you do it,> > >> you might begin to discover
just how much you really don't know, and> >> > >> > > something about
the things you think you know that just ain't so.>> > >> > > Population
genetics is mathematically difficult, and can be> > >> assisted by
computer simulation. Out of curiosity I've previously> > >> written a
program to explore population behaviour and allele fixation,> > >>
using recombination and various profiles of mutation selection> > >>
coefficients (i.e. assigning different probabilities to a range from> >
different definitions of genotype and phenotype?> > The problem with> >lethal to neutral to slightly positive).> > >> > > Do you have> > >>
natural> > >> selection has little to do with having an incorrectyour claim that topoisomerase mutations are beyond the reach of
definition of> > >> phenotype or genotype. The problem is your idea
that mutations that> > >> effect basic, internal cellular functions,
like DNA replication, or> > >> transcription, or formation of
chromatin, are somehow less accessible> > >> to natural selection than
genes that effect things like body mass, or> > >> coloration, or beak
shape. Any mutation that effects fitness in any> > >> way, no matter
where that effect occurs in the organism, is accessible> > >> to
natural selection. And no matter where in the organism the effect> > >>
occurs, there is always a long chain of effects between the mutation> >
special> > >> in that regard about mutations in topoisomerase genes.> >itself and whatever effect it has on fitness. There is nothing
positive> > >> selection pressure applied.>> The evolution ofTo repeat an example: the development of the camera-style eyes of> >
vertebrates requires gradual refinement over many steps with
Topoisomerase II may> > >> include some functional intermediates or it
may co-opt extant> > >> subcomponents, but either way, its high
informational and functional> > >> specificity and complexity will
similarly necessitate gradual> > >> refinement over many steps with
positive selection pressure applied.>>> > >> The evolutionary pathway
of an eye can be conceived of as a long series> > >> of small
variations each producing *functional* intermediates. But this> > >> is
much more difficult with the evolution of Topoisomerase II. Most> > >>
intermediates will be *non-functional* in terms of *progression
towards> > >> Topoisomerase II function*. That's the problem.> > > Why
do you think intermediates will be non-functional, even in terms of> >
progression to topoisomerase II function? That function requires> > >various enzymatic activities, various specific bindings. Why can't> > >
changes in the amino acid sequence (and hence the 3-d structure) lead>
biochemistry, and just repeats stuff> > he's found in creationistto slightly better substrate binding, slightly increased enzymatic>
activity, etc? How is this different than gradual refinement of
biological activity?> > The problem is that MarkE knows no
publications. It's probably a waste of time> > arfuing with him. So far
the specific point is concerned we *know* from> > Steve Benner's work
(on ribonuclease, for example) that the catalytic> > activity of
ancestral forms can be measured.
Actually, I think your problem is you really don't like anyone
challenging the naturalist position.
I've noticed your own tactic is either to not respond, or make
unsubstantiated dismissive remarks like this one. What is conspicuously
missing is a coherent and substantive critique of my proposition.
Rather, you offer a lazy "Steve Benner said...">>
Once more: the development of the camera-style eyes of vertebrates
requires gradual refinement over many steps with positive selection
pressure applied.
The evolution of Topoisomerase II may include some functional
intermediates or it may co-opt extant subcomponents, but either way,
its high informational and functional specificity and complexity will
similarly necessitate gradual refinement over many steps with positive
selection pressure applied.
The evolutionary pathway of an eye can be conceived of as a long series
of small variations each producing *functional* intermediates. But this
is much more difficult with the evolution of Topoisomerase II. Most
intermediates will be *non-functional* in terms of *progression towards
Topoisomerase II function*. Regardless of Steve Benner's work (on
ribonuclease, for example).>> That's the problem.
Except that you have not shown that it's a problem. Topoisomerase is an enzyme. Mutations in enzymes change their activity. What's problematic
about mutations gradually improving the activity of topoisomerase?
Given a choice between a barely active proto-topoisomerase and one that
is slightly more active, why couldn't natural selection select for the slightly more active one? You (or, more likely, your sources) are
inventing a problem that is not there.
On Friday, October 13, 2023 at 8:36:06?AM UTC-4, jillery wrote:incremental development of the camera-style eyes of vertebrates. In both examples, NS has direct “visibility” of the competing variants.
On Fri, 13 Oct 2023 03:55:13 -0700 (PDT), MarkE <me22...@gmail.com>
wrote:
On Thursday, October 12, 2023 at 10:16:06?PM UTC+11, Lawyer Daggett wrote: >> >> On Thursday, October 12, 2023 at 6:06:06?AM UTC-4, MarkE wrote:
NS acts on the phenotype, selecting on the basis of its traits or behaviours in a given environment. For example, Galapagos finches beak size selected as a result of the varying availability of large hard seeds or small soft seeds. Or the gradual,
From Oxford Languages:The above presses a gross misconception: that phenotype means "observable
anatomical feature" . You compound this gross misunderstanding below.
"phenotype: the set of observable characteristics of an individual
resulting from the interaction of its genotype with the environment."
Not sure what Daggett's objection is here.
That's a rotten definition, especially when you want to apply it scientifically.
It's rotten because so many will misunderstand "observable" to mean something >that you visually detect. If one has a more scientific notion of "observable" to
mean has a measurable effect, it's closer. A phenotype is a tangible consequence
of a genotype. It can be cryptic. A phenotype can produce improved resistance >to cold/heat, which won't be revealed outside of cold/hot conditions.
Regardless, it's clear MarkE was inclined to dismiss 'invisible' intracellular changes
as not being phenotype changes, which he thought couldn't be acted upon by >natural selection.
regions) is part of the phenotype, insofar as it is a dynamic, chemically active, physical structure. It follows from this that the genotype is non-physical information, which is embodied in DNA.Here’s the problem.
Human topoisomerase, for example, contains 765 amino acids. Topoisomerase II gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it has very high information content (765 units) and functional complexity and specificity.
But this is all happening inside the cell, out of the direct reach of NS.I'm cutting you off. Nobody, who has completed even a high school biology course,
has any excuse for that misconception. It's grotesquely wrong.
My question for you is, is that level of ignorance a proper foundation from
which to debate the validity of the theory of evolution? Son, people can see you.
Valid point - my premise should instead be stated something like this: "parts of the phenotype less accessible to natural selection". As regards the genotype/phenotype distinction, I would say that even the DNA itself (including protein coding
Stipulating for argument's sake that all you say above is technically
correct, what's your point in saying it? It doesn't challenge natural
selection. It doesn't support ID or Creationism. It's not an
especially significant biological fact.
It's technically false, except where it isn't even false because it's gibberish.
My question to you is, why the rage and vitriol?Since you asked, here's my guess:
<https://www.youtube.com/watch?v=aME0qvhZ37o>
As I used to have to say to my grandkids when they were little. Use your words.
On Saturday, October 14, 2023 at 9:56:08 AM UTC-4, MarkE wrote:coherent and substantive critique of my proposition. Rather, you offer a lazy "Steve Benner said..."
On Sunday, October 15, 2023 at 12:21:08 AM UTC+11, Athel Cornish-Bowden wrote:
On 2023-10-14 13:04:27 +0000, broger...@gmail.com said:
Actually, I think your problem is you really don't like anyone challenging the naturalist position. I've noticed your own tactic is either to not respond, or make unsubstantiated dismissive remarks like this one. What is conspicuously missing is aOn Saturday, October 14, 2023 at 8:26:07 AM UTC-4, MarkE wrote:The problem is that MarkE knows no biochemistry, and just repeats stuff he's found in creationist publications. It's probably a waste of time arfuing with him. So far the specific point is concerned we *know* from Steve Benner's work (on ribonuclease, for example) that the catalytic activity of ancestral forms can be measured.
On Saturday, October 14, 2023 at 11:16:08 PM UTC+11,Why do you think intermediates will be non-functional, even in terms of
broger...@gmail.com wrote:> > On Saturday, October 14, 2023 at 7:51:08
AM UTC-4, MarkE wrote:> > > On Friday, October 13, 2023 at 11:26:07 PM
UTC+11, Lawyer Daggett wrote:> > > > On Friday, October 13, 2023 at >> 6:56:06 AM UTC-4, MarkE wrote:> > > > > On Thursday, October 12, 2023
at 10:16:06 PM UTC+11, Lawyer Daggett wrote:> > > > > > On Thursday,
October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:> > > > > > > NS acts
on the phenotype, selecting on the basis of its traits or behaviours in
a given environment. For example, Galapagos finches beak size selected
as a result of the varying availability of large hard seeds or small >> soft seeds. Or the gradual, incremental development of the camera-style
eyes of vertebrates. In both examples, NS has direct “visibility” of
the competing variants.> > > > .> > > > > > The above presses a gross >> misconception: that phenotype means "observable> > > > > > anatomical >> feature" . You compound this gross misunderstanding below.> > > > .> >
topoisomerase, for example, contains 765 amino acids. Topoisomerase IIHere’s the problem.> > > > > > >> > > > > > > Human
gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it
has very high information content (765 units) and functional complexity
and specificity.> > > > > > >> > > > > > > But this is all happening >> inside the cell, out of the direct reach of NS.> > > > > > I'm cutting
you off. Nobody, who has completed even a high school biology course,>
wrong.> > > > > >> > > > > > My question for you is, is that level of >> ignorance a proper foundation from> > > > > > which to debate thehas any excuse for that misconception. It's grotesquely
validity of the theory of evolution? Son, people can see you.> > > >> >
this: "parts of the> > > > > phenotype less accessible to naturalValid point - my premise should instead be stated something like
selection". As regards the genotype/phenotype> > > > > distinction, I >> would say that even the DNA itself (including protein coding regions)>
chemically active, physical> > > > > structure. It follows from this >> that the genotype is non-physical information,> > > > > which isis part of the phenotype, insofar as it is a dynamic,
embodied in DNA.> > > > >> > > > > My question to you is, why the rage
and vitriol?> > > > You're "correction" is still loaded is falsehoods.
We're not talking about incorrect> > > > deductions. We're talking
about asserting false premises. It's bullshit.> > > >> > > > It makes >> it evident that you have almost no understanding of even the terms> > >
"phenotype", "selections", and as such no understanding ofevolution.> > > >> > > > Imagine you are an auto mechanic, somebody >> drops off their car for repair and> > > > you fix it. The car's
computer had thrown some codes about about misfiring and> > > >
problems with certain voltage on some fuel injectors. You know your >> stuff so> > > > you strip off the plenum and get to the injectors, you
take out your handy volt-ohm> > > > meter and check the resistance
across the indicated injector and it is a dead short.> > > >> > > > You
call up the customer and ask if they want you to go ahead and replace >> all of> > > >> > > > the injectors while you are there as the car has >> over 90K miles and it will save> > > > them a lot of money if you do >> them all now rather than have to do the tear down> > > > again for one
that will quite likely fail in the next 10-15K miles.> > > >> > > > He
gets upset and tells you you don't know what you're doing, you just >> need to> > > > clear the computer code so you could pass your state >> inspection. It was a computer> > > > problem, the engine was running >> fine. Sure, running fine with a fuel injector that> > > > was shorted >> out.> > > >> > > > The guy doesn't understand cars but he's telling you
what the problem is.> > > >> > > > The point is, you aren't seeing rage
and vitriol. You are seeing exasperation.> > > > You don't even
understand a simple thing like selection and you are here evangelizing>
be math, and> > > > lots of it. Not that you're ready for it, butabout how evolution could not have produced X, Y, or Z.> > > >> >Find an on-line course on population genetics. Take it. There will
you'll understand some of it. More significantly,> > > > if you do it,
you might begin to discover just how much you really don't know, and> >
assisted by computer simulation. Out of curiosity I've previouslysomething about the things you think you know that just ain't so.>
Population genetics is mathematically difficult, and can be
written a program to explore population behaviour and allele fixation,
using recombination and various profiles of mutation selection
coefficients (i.e. assigning different probabilities to a range from >> lethal to neutral to slightly positive).> > >> > > Do you have
different definitions of genotype and phenotype?> > The problem with >> your claim that topoisomerase mutations are beyond the reach of natural
selection has little to do with having an incorrect definition of
phenotype or genotype. The problem is your idea that mutations that >> effect basic, internal cellular functions, like DNA replication, or >> transcription, or formation of chromatin, are somehow less accessible >> to natural selection than genes that effect things like body mass, or >> coloration, or beak shape. Any mutation that effects fitness in any >> way, no matter where that effect occurs in the organism, is accessible
to natural selection. And no matter where in the organism the effect >> occurs, there is always a long chain of effects between the mutation >> itself and whatever effect it has on fitness. There is nothing special
in that regard about mutations in topoisomerase genes.
To repeat an example: the development of the camera-style eyes of
vertebrates requires gradual refinement over many steps with positive >> selection pressure applied.>> The evolution of Topoisomerase II may >> include some functional intermediates or it may co-opt extant
subcomponents, but either way, its high informational and functional >> specificity and complexity will similarly necessitate gradual
refinement over many steps with positive selection pressure applied.>>
The evolutionary pathway of an eye can be conceived of as a long series
of small variations each producing *functional* intermediates. But this
is much more difficult with the evolution of Topoisomerase II. Most >> intermediates will be *non-functional* in terms of *progression towards
Topoisomerase II function*. That's the problem.
progression to topoisomerase II function? That function requires various enzymatic activities, various specific bindings. Why can't changes in the amino acid sequence (and hence the 3-d structure) lead to slightly better substrate binding, slightly increased enzymatic activity, etc? How is this different than gradual refinement of any biological activity?
many steps with positive selection pressure applied.Once more: the development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.
The evolution of Topoisomerase II may include some functional intermediates or it may co-opt extant subcomponents, but either way, its high informational and functional specificity and complexity will similarly necessitate gradual refinement over
in terms of *progression towards Topoisomerase II function*. Regardless of Steve Benner's work (on ribonuclease, for example).The evolutionary pathway of an eye can be conceived of as a long series of small variations each producing *functional* intermediates. But this is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-functional*
proto-topoisomerase and one that is slightly more active, why couldn't natural selection select for the slightly more active one? You (or, more likely, your sources) are inventing a problem that is not there.That's the problem.Except that you have not shown that it's a problem. Topoisomerase is an enzyme. Mutations in enzymes change their activity. What's problematic about mutations gradually improving the activity of topoisomerase? Given a choice between a barely active
--
athel cb : Biochemical Evolution, Garland Science, 2016
On 14/10/2023 13:15, MarkE wrote:
Not so. I accepted the correction that these are indeed phenotype
changes (e.g. lactose metabolism in bacteria). But my argument is that substantial intracellular changes (what might be called "molecular macroevolution") may be less accessible to NS. For example, the development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.
The
evolution of Topoisomerase II may include some functional intermediates
or it may co-opt extant subcomponents, but either way, its informational and functional specificity and complexity will similarly necessitate gradual refinement over many steps with positive selection pressure applied.
The development pathway of an eye can be conceived as longThat's not what you seemed to be claiming before. You were claiming that
series of small variations each producing *functional* intermediates.
This is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-functional* in terms of progression towards Topoisomerase II function. That's the problem.
it wasn't accessible to natural selection. You're now claiming an
absence of functional intermediates, which is not the same thing. "Accessible to natural selection" and "accessible by natural selection"
may be only a small change in sequence, but it's a large change in semantics.
Anyway, creationists have long claimed that eyes are unevolvable due to
a putative lack of intermediates. Why should we take your claim about topoisomerases more seriously that their claims about eyes? Picking a
darker crevice (topoisomerases evolved longer ago, so more of the
evidence has been erased by time) for your gap doesn't make the argument better.
--
alias Ernest Major
On Sunday, October 15, 2023 at 2:16:08 AM UTC+11, broger...@gmail.com wrote:coherent and substantive critique of my proposition. Rather, you offer a lazy "Steve Benner said..."
On Saturday, October 14, 2023 at 9:56:08 AM UTC-4, MarkE wrote:
On Sunday, October 15, 2023 at 12:21:08 AM UTC+11, Athel Cornish-Bowden wrote:
On 2023-10-14 13:04:27 +0000, broger...@gmail.com said:
Actually, I think your problem is you really don't like anyone challenging the naturalist position. I've noticed your own tactic is either to not respond, or make unsubstantiated dismissive remarks like this one. What is conspicuously missing is aOn Saturday, October 14, 2023 at 8:26:07 AM UTC-4, MarkE wrote:The problem is that MarkE knows no biochemistry, and just repeats stuff
On Saturday, October 14, 2023 at 11:16:08 PM UTC+11,Why do you think intermediates will be non-functional, even in terms of
broger...@gmail.com wrote:> > On Saturday, October 14, 2023 at 7:51:08
AM UTC-4, MarkE wrote:> > > On Friday, October 13, 2023 at 11:26:07 PM
UTC+11, Lawyer Daggett wrote:> > > > On Friday, October 13, 2023 at >> 6:56:06 AM UTC-4, MarkE wrote:> > > > > On Thursday, October 12, 2023
at 10:16:06 PM UTC+11, Lawyer Daggett wrote:> > > > > > On Thursday,
October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:> > > > > > > NS acts
on the phenotype, selecting on the basis of its traits or behaviours in
a given environment. For example, Galapagos finches beak size selected
as a result of the varying availability of large hard seeds or small
soft seeds. Or the gradual, incremental development of the camera-style
eyes of vertebrates. In both examples, NS has direct “visibility” of
the competing variants.> > > > .> > > > > > The above presses a gross
misconception: that phenotype means "observable> > > > > > anatomical
feature" . You compound this gross misunderstanding below.> > > > .> >
topoisomerase, for example, contains 765 amino acids. Topoisomerase IIHere’s the problem.> > > > > > >> > > > > > > Human
gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, it
has very high information content (765 units) and functional complexity
and specificity.> > > > > > >> > > > > > > But this is all happening
inside the cell, out of the direct reach of NS.> > > > > > I'm cutting
you off. Nobody, who has completed even a high school biology course,>
ignorance a proper foundation from> > > > > > which to debate the >> validity of the theory of evolution? Son, people can see you.> > > >> >has any excuse for that misconception. It's grotesquely >> wrong.> > > > > >> > > > > > My question for you is, is that level of
this: "parts of the> > > > > phenotype less accessible to natural >> selection". As regards the genotype/phenotype> > > > > distinction, IValid point - my premise should instead be stated something like
would say that even the DNA itself (including protein coding regions)>
chemically active, physical> > > > > structure. It follows from thisis part of the phenotype, insofar as it is a dynamic,
that the genotype is non-physical information,> > > > > which is
embodied in DNA.> > > > >> > > > > My question to you is, why the rage
and vitriol?> > > > You're "correction" is still loaded is falsehoods.
We're not talking about incorrect> > > > deductions. We're talking >> about asserting false premises. It's bullshit.> > > >> > > > It makes
it evident that you have almost no understanding of even the terms> > >
"phenotype", "selections", and as such no understanding ofevolution.> > > >> > > > Imagine you are an auto mechanic, somebody >> drops off their car for repair and> > > > you fix it. The car's
computer had thrown some codes about about misfiring and> > > >
problems with certain voltage on some fuel injectors. You know your >> stuff so> > > > you strip off the plenum and get to the injectors, you
take out your handy volt-ohm> > > > meter and check the resistance >> across the indicated injector and it is a dead short.> > > >> > > > You
call up the customer and ask if they want you to go ahead and replace
all of> > > >> > > > the injectors while you are there as the car has
over 90K miles and it will save> > > > them a lot of money if you do
them all now rather than have to do the tear down> > > > again for one
that will quite likely fail in the next 10-15K miles.> > > >> > > > He
gets upset and tells you you don't know what you're doing, you just >> need to> > > > clear the computer code so you could pass your state >> inspection. It was a computer> > > > problem, the engine was running
fine. Sure, running fine with a fuel injector that> > > > was shorted
out.> > > >> > > > The guy doesn't understand cars but he's telling you
what the problem is.> > > >> > > > The point is, you aren't seeing rage
and vitriol. You are seeing exasperation.> > > > You don't even
understand a simple thing like selection and you are here evangelizing>
be math, and> > > > lots of it. Not that you're ready for it, but >> you'll understand some of it. More significantly,> > > > if you do it,about how evolution could not have produced X, Y, or Z.> > > >> >Find an on-line course on population genetics. Take it. There will
you might begin to discover just how much you really don't know, and> >
assisted by computer simulation. Out of curiosity I've previously >> written a program to explore population behaviour and allele fixation,something about the things you think you know that just ain't so.>
Population genetics is mathematically difficult, and can be
using recombination and various profiles of mutation selection
coefficients (i.e. assigning different probabilities to a range from
lethal to neutral to slightly positive).> > >> > > Do you have
different definitions of genotype and phenotype?> > The problem with
your claim that topoisomerase mutations are beyond the reach of natural
selection has little to do with having an incorrect definition of >> phenotype or genotype. The problem is your idea that mutations that >> effect basic, internal cellular functions, like DNA replication, or >> transcription, or formation of chromatin, are somehow less accessible
to natural selection than genes that effect things like body mass, or
coloration, or beak shape. Any mutation that effects fitness in any >> way, no matter where that effect occurs in the organism, is accessible
to natural selection. And no matter where in the organism the effect
occurs, there is always a long chain of effects between the mutation
itself and whatever effect it has on fitness. There is nothing special
in that regard about mutations in topoisomerase genes.
To repeat an example: the development of the camera-style eyes of >> vertebrates requires gradual refinement over many steps with positive
selection pressure applied.>> The evolution of Topoisomerase II may >> include some functional intermediates or it may co-opt extant
subcomponents, but either way, its high informational and functional
specificity and complexity will similarly necessitate gradual
refinement over many steps with positive selection pressure applied.>>
The evolutionary pathway of an eye can be conceived of as a long series
of small variations each producing *functional* intermediates. But this
is much more difficult with the evolution of Topoisomerase II. Most >> intermediates will be *non-functional* in terms of *progression towards
Topoisomerase II function*. That's the problem.
progression to topoisomerase II function? That function requires various enzymatic activities, various specific bindings. Why can't changes in the amino acid sequence (and hence the 3-d structure) lead
to slightly better substrate binding, slightly increased enzymatic activity, etc? How is this different than gradual refinement of any biological activity?
he's found in creationist publications. It's probably a waste of time arfuing with him. So far the specific point is concerned we *know* from
Steve Benner's work (on ribonuclease, for example) that the catalytic activity of ancestral forms can be measured.
many steps with positive selection pressure applied.Once more: the development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.
The evolution of Topoisomerase II may include some functional intermediates or it may co-opt extant subcomponents, but either way, its high informational and functional specificity and complexity will similarly necessitate gradual refinement over
functional* in terms of *progression towards Topoisomerase II function*. Regardless of Steve Benner's work (on ribonuclease, for example).The evolutionary pathway of an eye can be conceived of as a long series of small variations each producing *functional* intermediates. But this is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-
proto-topoisomerase and one that is slightly more active, why couldn't natural selection select for the slightly more active one? You (or, more likely, your sources) are inventing a problem that is not there.That's the problem.Except that you have not shown that it's a problem. Topoisomerase is an enzyme. Mutations in enzymes change their activity. What's problematic about mutations gradually improving the activity of topoisomerase? Given a choice between a barely active
The enzymatic activity here is not simple catalysis that lends itself to gradual improvements and reaction efficiency.ligation, and release).
In this case, it's the action of a molecular machine that is complex (765 amino acids) and specialised (it catalyses changes in DNA topology by passing one double-stranded DNA segment through another, which includes strand capture, cleavage, swapping,
Even if some subunits are preexisting, an evolutionary process would be required to integrate each subunit and control the new function (e.g. alterations to existing polymers to adapt them to the new ensemble, and additional amino acids to providecoordination).
I guess this comes down to familiar questions of a plausible gradual pathway and avoidance of irreducible complexity (the latter being a subset of the former?).
--
athel cb : Biochemical Evolution, Garland Science, 2016
On Sunday, October 15, 2023 at 2:26:07 AM UTC+11, Ernest Major wrote:probabilities associated with proposed solutions.
On 14/10/2023 13:15, MarkE wrote:
Not so. I accepted the correction that these are indeed phenotype changes (e.g. lactose metabolism in bacteria). But my argument is that substantial intracellular changes (what might be called "molecular macroevolution") may be less accessible to NS. For example, the development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.
The
evolution of Topoisomerase II may include some functional intermediates or it may co-opt extant subcomponents, but either way, its informational and functional specificity and complexity will similarly necessitate gradual refinement over many steps with positive selection pressure applied.
Further reflection makes me wonder if much/all of this debate is variations on / specific instances of (i) a plausible gradual pathway and (ii) avoidance of irreducible complexity (the latter being a subset of the former?), with evaluation ofThe development pathway of an eye can be conceived as longThat's not what you seemed to be claiming before. You were claiming that it wasn't accessible to natural selection. You're now claiming an
series of small variations each producing *functional* intermediates. This is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-functional* in terms of progression towards Topoisomerase II function. That's the problem.
absence of functional intermediates, which is not the same thing. "Accessible to natural selection" and "accessible by natural selection" may be only a small change in sequence, but it's a large change in semantics.
Anyway, creationists have long claimed that eyes are unevolvable due to
a putative lack of intermediates. Why should we take your claim about topoisomerases more seriously that their claims about eyes? Picking a darker crevice (topoisomerases evolved longer ago, so more of the
evidence has been erased by time) for your gap doesn't make the argument better.
--
alias Ernest Major
"selection" implies a conscious decision similar to how "design"
implies a designer, among those who believe in magic.
jillery wrote:
"selection" implies a conscious decision similar to how "design"
implies a designer, among those who believe in magic.
If you went on to say that "People who believe in magic" are those
who say things like "Selection" and "Design," you'd be correct.
On Sunday, October 15, 2023 at 10:46:09 PM UTC+11, broger...@gmail.com wrote:is a coherent and substantive critique of my proposition. Rather, you offer a lazy "Steve Benner said..."
On Sunday, October 15, 2023 at 7:06:09 AM UTC-4, MarkE wrote:
On Sunday, October 15, 2023 at 2:16:08 AM UTC+11, broger...@gmail.com wrote:
On Saturday, October 14, 2023 at 9:56:08 AM UTC-4, MarkE wrote:
On Sunday, October 15, 2023 at 12:21:08 AM UTC+11, Athel Cornish-Bowden wrote:
On 2023-10-14 13:04:27 +0000, broger...@gmail.com said:
Actually, I think your problem is you really don't like anyone challenging the naturalist position. I've noticed your own tactic is either to not respond, or make unsubstantiated dismissive remarks like this one. What is conspicuously missingOn Saturday, October 14, 2023 at 8:26:07 AM UTC-4, MarkE wrote:The problem is that MarkE knows no biochemistry, and just repeats stuff
On Saturday, October 14, 2023 at 11:16:08 PM UTC+11,Why do you think intermediates will be non-functional, even in terms of
broger...@gmail.com wrote:> > On Saturday, October 14, 2023 at 7:51:08
AM UTC-4, MarkE wrote:> > > On Friday, October 13, 2023 at 11:26:07 PM
UTC+11, Lawyer Daggett wrote:> > > > On Friday, October 13, 2023 at
6:56:06 AM UTC-4, MarkE wrote:> > > > > On Thursday, October 12, 2023
at 10:16:06 PM UTC+11, Lawyer Daggett wrote:> > > > > > On Thursday,
October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:> > > > > > > NS acts
on the phenotype, selecting on the basis of its traits or behaviours in
a given environment. For example, Galapagos finches beak size selected
as a result of the varying availability of large hard seeds or small
soft seeds. Or the gradual, incremental development of the camera-style
eyes of vertebrates. In both examples, NS has direct “visibility” of
the competing variants.> > > > .> > > > > > The above presses a gross
misconception: that phenotype means "observable> > > > > > anatomical
feature" . You compound this gross misunderstanding below.> > > > .> >
gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, itHere’s the problem.> > > > > > >> > > > > > > Human >> topoisomerase, for example, contains 765 amino acids. Topoisomerase II
has very high information content (765 units) and functional complexity
and specificity.> > > > > > >> > > > > > > But this is all happening
inside the cell, out of the direct reach of NS.> > > > > > I'm cutting
you off. Nobody, who has completed even a high school biology course,>
wrong.> > > > > >> > > > > > My question for you is, is that level ofhas any excuse for that misconception. It's grotesquely
ignorance a proper foundation from> > > > > > which to debate the
validity of the theory of evolution? Son, people can see you.> > > >> >
this: "parts of the> > > > > phenotype less accessible to naturalValid point - my premise should instead be stated something like
selection". As regards the genotype/phenotype> > > > > distinction, I
would say that even the DNA itself (including protein coding regions)>
that the genotype is non-physical information,> > > > > which isis part of the phenotype, insofar as it is a dynamic, >> chemically active, physical> > > > > structure. It follows from this
embodied in DNA.> > > > >> > > > > My question to you is, why the rage
and vitriol?> > > > You're "correction" is still loaded is falsehoods.
We're not talking about incorrect> > > > deductions. We're talking
about asserting false premises. It's bullshit.> > > >> > > > It makes
it evident that you have almost no understanding of even the terms> > >
"phenotype", "selections", and as such no understanding ofevolution.> > > >> > > > Imagine you are an auto mechanic, somebody
drops off their car for repair and> > > > you fix it. The car's >> computer had thrown some codes about about misfiring and> > > > >> problems with certain voltage on some fuel injectors. You know your
stuff so> > > > you strip off the plenum and get to the injectors, you
take out your handy volt-ohm> > > > meter and check the resistance
across the indicated injector and it is a dead short.> > > >> > > > You
call up the customer and ask if they want you to go ahead and replace
all of> > > >> > > > the injectors while you are there as the car has
over 90K miles and it will save> > > > them a lot of money if you do
them all now rather than have to do the tear down> > > > again for one
that will quite likely fail in the next 10-15K miles.> > > >> > > > He
gets upset and tells you you don't know what you're doing, you just
need to> > > > clear the computer code so you could pass your state
inspection. It was a computer> > > > problem, the engine was running
fine. Sure, running fine with a fuel injector that> > > > was shorted
out.> > > >> > > > The guy doesn't understand cars but he's telling you
what the problem is.> > > >> > > > The point is, you aren't seeing rage
and vitriol. You are seeing exasperation.> > > > You don't even >> understand a simple thing like selection and you are here evangelizing>
be math, and> > > > lots of it. Not that you're ready for it, butabout how evolution could not have produced X, Y, or Z.> > > >> >Find an on-line course on population genetics. Take it. There will
you'll understand some of it. More significantly,> > > > if you do it,
you might begin to discover just how much you really don't know, and> >
written a program to explore population behaviour and allele fixation,something about the things you think you know that just ain't so.>
Population genetics is mathematically difficult, and can be >> assisted by computer simulation. Out of curiosity I've previously
using recombination and various profiles of mutation selection >> coefficients (i.e. assigning different probabilities to a range from
lethal to neutral to slightly positive).> > >> > > Do you have >> different definitions of genotype and phenotype?> > The problem with
your claim that topoisomerase mutations are beyond the reach of natural
selection has little to do with having an incorrect definition of
phenotype or genotype. The problem is your idea that mutations that
effect basic, internal cellular functions, like DNA replication, or
transcription, or formation of chromatin, are somehow less accessible
to natural selection than genes that effect things like body mass, or
coloration, or beak shape. Any mutation that effects fitness in any
way, no matter where that effect occurs in the organism, is accessible
to natural selection. And no matter where in the organism the effect
occurs, there is always a long chain of effects between the mutation
itself and whatever effect it has on fitness. There is nothing special
in that regard about mutations in topoisomerase genes.
To repeat an example: the development of the camera-style eyes of
vertebrates requires gradual refinement over many steps with positive
selection pressure applied.>> The evolution of Topoisomerase II may
include some functional intermediates or it may co-opt extant >> subcomponents, but either way, its high informational and functional
specificity and complexity will similarly necessitate gradual >> refinement over many steps with positive selection pressure applied.>>
The evolutionary pathway of an eye can be conceived of as a long series
of small variations each producing *functional* intermediates. But this
is much more difficult with the evolution of Topoisomerase II. Most
intermediates will be *non-functional* in terms of *progression towards
Topoisomerase II function*. That's the problem.
progression to topoisomerase II function? That function requires various enzymatic activities, various specific bindings. Why can't
changes in the amino acid sequence (and hence the 3-d structure) lead
to slightly better substrate binding, slightly increased enzymatic
activity, etc? How is this different than gradual refinement of any
biological activity?
he's found in creationist publications. It's probably a waste of time
arfuing with him. So far the specific point is concerned we *know* from
Steve Benner's work (on ribonuclease, for example) that the catalytic
activity of ancestral forms can be measured.
over many steps with positive selection pressure applied.Once more: the development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.
The evolution of Topoisomerase II may include some functional intermediates or it may co-opt extant subcomponents, but either way, its high informational and functional specificity and complexity will similarly necessitate gradual refinement
functional* in terms of *progression towards Topoisomerase II function*. Regardless of Steve Benner's work (on ribonuclease, for example).The evolutionary pathway of an eye can be conceived of as a long series of small variations each producing *functional* intermediates. But this is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-
active proto-topoisomerase and one that is slightly more active, why couldn't natural selection select for the slightly more active one? You (or, more likely, your sources) are inventing a problem that is not there.That's the problem.Except that you have not shown that it's a problem. Topoisomerase is an enzyme. Mutations in enzymes change their activity. What's problematic about mutations gradually improving the activity of topoisomerase? Given a choice between a barely
swapping, ligation, and release).The enzymatic activity here is not simple catalysis that lends itself to gradual improvements and reaction efficiency.
In this case, it's the action of a molecular machine that is complex (765 amino acids) and specialised (it catalyses changes in DNA topology by passing one double-stranded DNA segment through another, which includes strand capture, cleavage,
coordination).There are lots of big enzymes and enzyme complexes which catalyze multi-step processes. Why do you think topoisomerase is special?
Even if some subunits are preexisting, an evolutionary process would be required to integrate each subunit and control the new function (e.g. alterations to existing polymers to adapt them to the new ensemble, and additional amino acids to provide
biology text on the way to get enough background that the papers on topoisomerase evolution would make sense to you.I guess this comes down to familiar questions of a plausible gradual pathway and avoidance of irreducible complexity (the latter being a subset of the former?).Sure. And if you were interested, you could go to Google Scholar and search on evolution of topoisomerases (and gyrases) and try to figure out what is already known in terms of possible intermediates, etc. You might have to stop by a molecular
supernatural) designer." But that sort of argument is useless both scientifically and theologically.The much bigger question is why are you wasting your time with this stuff? It is beyond obvious that your main interest in any of this, OoL or topoisomerase evolution is to say "look, science has no explanation for this, therefore there is a (
answer, give up." Supernatural ID provides no details and is supported by no direct evidence - indeed you say yourself that it would be a category error to ask such things of supernatural ID. So it gets you nowhere in terms of understanding the whatSupernatural ID is useless scientifically because it leads nowhere. All it does is say - "If you've been trying to understand something for X amount of time and have had Y amount of resources available to you, and you still don't have a definitive
There is not unlimited time and space to overcome the improbability of naturalistic OoL and evolution. Creationist arguments that appeal to science attempt show that naturalism has exceeded its budget.
You are in effect saying that the creation vs OoL/evolution debate is invalid. You'd be much happier posting to talk.only_naturalistic_origins
prosper. The race does not go to the swift. But, the indifference is an illusion. God is not indifferent to human suffering, indeed He became a human and suffered terribly and unjustly. He knows what you are going through, and He says "Have faith. LoveMore importantly, supernatural ID is useless theologically. Remember your favorite Dawkins quote about how the universe looks like it has nothing but blind, pitiless indifference to anything we care about. Well, here are two potential rebuttals.
1. More or less mainstream Christian rebuttal: Yes, the universe can look pitiless and indifferent to human suffering, especially the suffering of the innocent. Children die of cancer, good, generous people die in natural disasters while the wicked
processes, bacterial flagella, metazoan body plans. So there must be an intelligent designer behind it all. We cannot draw any conclusions about the designer apart from the things he designed. So we know that the designer designed a universe that acts2. Supernatural ID rebuttal: Yes, the universe looks pitiless and indifferent. But it also contains a lot of complicated stuff in it that could not have occurred naturally - finely tuned constants of nature, the origin of life, multi-step enzyme
died as long as you sincerely believe. For that you need a leap of faith. And that leap of faith is no bigger or smaller depending on whether you are satisfied with progress in OoL research or topoisomerase evolution.Supernatural ID does not get you to the sort of God you want to believe in - an invisible, omnipotent, personal loving God who cares for you and everybody else and offers you eternal life and the chance to reconnect with all your loved ones who have
with science as totally irrelevant. Nobody accepts Jesus Christ as their personal Lord and Savior because he offers a better explanation of the OoL than David Deamer. And a fully worked out empirically supported naturalistic explanation for the OoL wouldIf you want to understand evolutionary biology and molecular biology and genetics, you need to go take some courses or at least work through a few textbooks. If you want to work on Rebuttal #1, though, you can skip right over anything having to do
--
athel cb : Biochemical Evolution, Garland Science, 2016
On Sunday, October 15, 2023 at 7:06:09 AM UTC-4, MarkE wrote:a coherent and substantive critique of my proposition. Rather, you offer a lazy "Steve Benner said..."
On Sunday, October 15, 2023 at 2:16:08 AM UTC+11, broger...@gmail.com wrote:
On Saturday, October 14, 2023 at 9:56:08 AM UTC-4, MarkE wrote:
On Sunday, October 15, 2023 at 12:21:08 AM UTC+11, Athel Cornish-Bowden wrote:
On 2023-10-14 13:04:27 +0000, broger...@gmail.com said:
Actually, I think your problem is you really don't like anyone challenging the naturalist position. I've noticed your own tactic is either to not respond, or make unsubstantiated dismissive remarks like this one. What is conspicuously missing isOn Saturday, October 14, 2023 at 8:26:07 AM UTC-4, MarkE wrote:The problem is that MarkE knows no biochemistry, and just repeats stuff
On Saturday, October 14, 2023 at 11:16:08 PM UTC+11,Why do you think intermediates will be non-functional, even in terms of
broger...@gmail.com wrote:> > On Saturday, October 14, 2023 at 7:51:08
AM UTC-4, MarkE wrote:> > > On Friday, October 13, 2023 at 11:26:07 PM
UTC+11, Lawyer Daggett wrote:> > > > On Friday, October 13, 2023 at
6:56:06 AM UTC-4, MarkE wrote:> > > > > On Thursday, October 12, 2023
at 10:16:06 PM UTC+11, Lawyer Daggett wrote:> > > > > > On Thursday,
October 12, 2023 at 6:06:06 AM UTC-4, MarkE wrote:> > > > > > > NS acts
on the phenotype, selecting on the basis of its traits or behaviours in
a given environment. For example, Galapagos finches beak size selected
as a result of the varying availability of large hard seeds or small
soft seeds. Or the gradual, incremental development of the camera-style
eyes of vertebrates. In both examples, NS has direct “visibility” of
the competing variants.> > > > .> > > > > > The above presses a gross
misconception: that phenotype means "observable> > > > > > anatomical
feature" . You compound this gross misunderstanding below.> > > > .> >
gathers, clamps, snips, swaps, and rejoins DNA strands [1]. That is, itHere’s the problem.> > > > > > >> > > > > > > Human >> topoisomerase, for example, contains 765 amino acids. Topoisomerase II
has very high information content (765 units) and functional complexity
and specificity.> > > > > > >> > > > > > > But this is all happening
inside the cell, out of the direct reach of NS.> > > > > > I'm cutting
you off. Nobody, who has completed even a high school biology course,>
ignorance a proper foundation from> > > > > > which to debate the >> validity of the theory of evolution? Son, people can see you.> > > >> >has any excuse for that misconception. It's grotesquely >> wrong.> > > > > >> > > > > > My question for you is, is that level of
this: "parts of the> > > > > phenotype less accessible to natural >> selection". As regards the genotype/phenotype> > > > > distinction, IValid point - my premise should instead be stated something like
would say that even the DNA itself (including protein coding regions)>
chemically active, physical> > > > > structure. It follows from thisis part of the phenotype, insofar as it is a dynamic,
that the genotype is non-physical information,> > > > > which is >> embodied in DNA.> > > > >> > > > > My question to you is, why the rage
and vitriol?> > > > You're "correction" is still loaded is falsehoods.
We're not talking about incorrect> > > > deductions. We're talking
about asserting false premises. It's bullshit.> > > >> > > > It makes
it evident that you have almost no understanding of even the terms> > >
"phenotype", "selections", and as such no understanding ofevolution.> > > >> > > > Imagine you are an auto mechanic, somebody
drops off their car for repair and> > > > you fix it. The car's >> computer had thrown some codes about about misfiring and> > > > >> problems with certain voltage on some fuel injectors. You know your
stuff so> > > > you strip off the plenum and get to the injectors, you
take out your handy volt-ohm> > > > meter and check the resistance
across the indicated injector and it is a dead short.> > > >> > > > You
call up the customer and ask if they want you to go ahead and replace
all of> > > >> > > > the injectors while you are there as the car has
over 90K miles and it will save> > > > them a lot of money if you do
them all now rather than have to do the tear down> > > > again for one
that will quite likely fail in the next 10-15K miles.> > > >> > > > He
gets upset and tells you you don't know what you're doing, you just
need to> > > > clear the computer code so you could pass your state
inspection. It was a computer> > > > problem, the engine was running
fine. Sure, running fine with a fuel injector that> > > > was shorted
out.> > > >> > > > The guy doesn't understand cars but he's telling you
what the problem is.> > > >> > > > The point is, you aren't seeing rage
and vitriol. You are seeing exasperation.> > > > You don't even >> understand a simple thing like selection and you are here evangelizing>
be math, and> > > > lots of it. Not that you're ready for it, but >> you'll understand some of it. More significantly,> > > > if you do it,about how evolution could not have produced X, Y, or Z.> > > >> >Find an on-line course on population genetics. Take it. There will
you might begin to discover just how much you really don't know, and> >
using recombination and various profiles of mutation selectionsomething about the things you think you know that just ain't so.>
Population genetics is mathematically difficult, and can be >> assisted by computer simulation. Out of curiosity I've previously >> written a program to explore population behaviour and allele fixation,
coefficients (i.e. assigning different probabilities to a range from
lethal to neutral to slightly positive).> > >> > > Do you have
different definitions of genotype and phenotype?> > The problem with
your claim that topoisomerase mutations are beyond the reach of natural
selection has little to do with having an incorrect definition of >> phenotype or genotype. The problem is your idea that mutations that
effect basic, internal cellular functions, like DNA replication, or
transcription, or formation of chromatin, are somehow less accessible
to natural selection than genes that effect things like body mass, or
coloration, or beak shape. Any mutation that effects fitness in any
way, no matter where that effect occurs in the organism, is accessible
to natural selection. And no matter where in the organism the effect
occurs, there is always a long chain of effects between the mutation
itself and whatever effect it has on fitness. There is nothing special
in that regard about mutations in topoisomerase genes.
To repeat an example: the development of the camera-style eyes of >> vertebrates requires gradual refinement over many steps with positive
selection pressure applied.>> The evolution of Topoisomerase II may
include some functional intermediates or it may co-opt extant
subcomponents, but either way, its high informational and functional
specificity and complexity will similarly necessitate gradual
refinement over many steps with positive selection pressure applied.>>
The evolutionary pathway of an eye can be conceived of as a long series
of small variations each producing *functional* intermediates. But this
is much more difficult with the evolution of Topoisomerase II. Most
intermediates will be *non-functional* in terms of *progression towards
Topoisomerase II function*. That's the problem.
progression to topoisomerase II function? That function requires various enzymatic activities, various specific bindings. Why can't changes in the amino acid sequence (and hence the 3-d structure) lead
to slightly better substrate binding, slightly increased enzymatic activity, etc? How is this different than gradual refinement of any
biological activity?
he's found in creationist publications. It's probably a waste of time
arfuing with him. So far the specific point is concerned we *know* from
Steve Benner's work (on ribonuclease, for example) that the catalytic
activity of ancestral forms can be measured.
many steps with positive selection pressure applied.Once more: the development of the camera-style eyes of vertebrates requires gradual refinement over many steps with positive selection pressure applied.
The evolution of Topoisomerase II may include some functional intermediates or it may co-opt extant subcomponents, but either way, its high informational and functional specificity and complexity will similarly necessitate gradual refinement over
functional* in terms of *progression towards Topoisomerase II function*. Regardless of Steve Benner's work (on ribonuclease, for example).The evolutionary pathway of an eye can be conceived of as a long series of small variations each producing *functional* intermediates. But this is much more difficult with the evolution of Topoisomerase II. Most intermediates will be *non-
proto-topoisomerase and one that is slightly more active, why couldn't natural selection select for the slightly more active one? You (or, more likely, your sources) are inventing a problem that is not there.That's the problem.Except that you have not shown that it's a problem. Topoisomerase is an enzyme. Mutations in enzymes change their activity. What's problematic about mutations gradually improving the activity of topoisomerase? Given a choice between a barely active
ligation, and release).The enzymatic activity here is not simple catalysis that lends itself to gradual improvements and reaction efficiency.
In this case, it's the action of a molecular machine that is complex (765 amino acids) and specialised (it catalyses changes in DNA topology by passing one double-stranded DNA segment through another, which includes strand capture, cleavage, swapping,
There are lots of big enzymes and enzyme complexes which catalyze multi-step processes. Why do you think topoisomerase is special?coordination).
Even if some subunits are preexisting, an evolutionary process would be required to integrate each subunit and control the new function (e.g. alterations to existing polymers to adapt them to the new ensemble, and additional amino acids to provide
text on the way to get enough background that the papers on topoisomerase evolution would make sense to you.I guess this comes down to familiar questions of a plausible gradual pathway and avoidance of irreducible complexity (the latter being a subset of the former?).Sure. And if you were interested, you could go to Google Scholar and search on evolution of topoisomerases (and gyrases) and try to figure out what is already known in terms of possible intermediates, etc. You might have to stop by a molecular biology
The much bigger question is why are you wasting your time with this stuff? It is beyond obvious that your main interest in any of this, OoL or topoisomerase evolution is to say "look, science has no explanation for this, therefore there is a (supernatural) designer." But that sort of argument is useless both scientifically and theologically.
Supernatural ID is useless scientifically because it leads nowhere. All it does is say - "If you've been trying to understand something for X amount of time and have had Y amount of resources available to you, and you still don't have a definitiveanswer, give up." Supernatural ID provides no details and is supported by no direct evidence - indeed you say yourself that it would be a category error to ask such things of supernatural ID. So it gets you nowhere in terms of understanding the what
More importantly, supernatural ID is useless theologically. Remember your favorite Dawkins quote about how the universe looks like it has nothing but blind, pitiless indifference to anything we care about. Well, here are two potential rebuttals.prosper. The race does not go to the swift. But, the indifference is an illusion. God is not indifferent to human suffering, indeed He became a human and suffered terribly and unjustly. He knows what you are going through, and He says "Have faith. Love
1. More or less mainstream Christian rebuttal: Yes, the universe can look pitiless and indifferent to human suffering, especially the suffering of the innocent. Children die of cancer, good, generous people die in natural disasters while the wicked
2. Supernatural ID rebuttal: Yes, the universe looks pitiless and indifferent. But it also contains a lot of complicated stuff in it that could not have occurred naturally - finely tuned constants of nature, the origin of life, multi-step enzymeprocesses, bacterial flagella, metazoan body plans. So there must be an intelligent designer behind it all. We cannot draw any conclusions about the designer apart from the things he designed. So we know that the designer designed a universe that acts
Supernatural ID does not get you to the sort of God you want to believe in - an invisible, omnipotent, personal loving God who cares for you and everybody else and offers you eternal life and the chance to reconnect with all your loved ones who havedied as long as you sincerely believe. For that you need a leap of faith. And that leap of faith is no bigger or smaller depending on whether you are satisfied with progress in OoL research or topoisomerase evolution.
If you want to understand evolutionary biology and molecular biology and genetics, you need to go take some courses or at least work through a few textbooks. If you want to work on Rebuttal #1, though, you can skip right over anything having to do withscience as totally irrelevant. Nobody accepts Jesus Christ as their personal Lord and Savior because he offers a better explanation of the OoL than David Deamer. And a fully worked out empirically supported naturalistic explanation for the OoL would not
--
athel cb : Biochemical Evolution, Garland Science, 2016
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