Why “cellular”?
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Be fair, he may not be pretending. If he has drunk deeply from the well of ‘intelligent design’ writings (which his use if their terminology indicates) he may have been seriously misled about how science is done and know no better.
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@Midhun It might be helpful to step back from argument and discuss your understanding of terminology. Until we have some agreement on basic meaning it’s hard to make any progress.
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You stated:
If mutations are caused by cellular physiology that does not stop them from being random with respect to fitness.
Those are random mutations. Expressing an error prone polymerase that produces more random mutations does not make them non-random mutations.
If a poor person buys more lottery tickets than a rich person this does not make the lottery non-random.
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The fact that some of the mutations do not contribute to adaptation is how we know they’re random. If the mechanism somehow “knew” beforehand which mutations would produce the adaptation in question, there’d be no reason to generate huge numbers of them with no adaptive benefit, and it could just force only those that produced fitness gains to occur.
Again, only a minority produce anti-biotic resistance, the majority to not. They’re all random, and only because large numbers are produced are the adaptive ones found in the time allotted to the experiment.
It is the fact that the error-prone polymerases activated by the SOS response produces extraordinarily many copying errors that ensures this rate is high enough for those mutations to occur in that time. They are no less “accidents”, “errors”, “mistakes”, nor no less random with respect to fitness than the background rate produced by the less-error-prone polymerases normally responsible for DNA replication. All that changed was the rate at which these “accidents”, “errors”, “mistakes”, or whatever you want to call them, occurs.
On a related note, the background rate of mutation is ALSO influenced by “cellular physiology”. Everything present inside the cell has some sort of influence on the types and distributions of mutations that occur, though in most cases those effects are considerably weaker than the change in rate that results from an active SOS response.
UV radiation, besides directly damaging DNA, can also damage other things inside the cell and produce free radicals, which in turn can also chemically alter the DNA and produce mutations. That too would be “things inside the cellular physiology” resulting in mutations. The fact that an external influence (UV radiation) affected something inside the cell first is irrelevant. The result is the same: more mutations.
Exactly. These concepts were understood even before the structure and function of DNA was fully developed.
The classic random mutation papers:
Plate replica experiment (Lederbergs):
Fluctuation assay (Luria and Delbruck, awarded Nobel Prize):
If memory serves, the SOS response was discovered in part because of experiments that hinted at non-random mutations. In certain experiments, they were seeing higher than normal lac+ revertants which suggested that a beneficial mutation was occurring more often than it should. However, they soon found that they were seeing the induction of a higher mutation rate which explained why they were seeing higher than expected lac+ revertants.
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It’s probably not the first, but this is one nice study that shows that adaptive (induced) mutations do not target exclusively genes whose changes would provide benefits:
The abstract:
“Stationary-phase mutation in microbes can produce selected (‘adaptive’) mutants preferentially. In one system, this occurs via a distinct, recombination-dependent mechanism. Two points of controversy have surrounded these adaptive reversions of an Escherichia coli lac mutation. First, are the mutations directed preferentially to the selected gene in a Lamarckian manner? Second, is the adaptive mutation mechanism specific to the F plasmid replicon carrying lac? We report that lac adaptive mutations are associated with hypermutation in unselected genes, in all replicons in the cell. The associated mutations have a similar sequence spectrum to the adaptive reversions. Thus, the adaptive mutagenesis mechanism is not directed to the lac genes, in a Lamarckian manner, nor to the F’ replicon carrying lac. Hypermutation was not found in non-revertants exposed to selection. Therefore, the genome-wide hypermutation underlying adaptive mutation occurs in a differentiated subpopulation. The existence of mutable subpopulations in non-growing cells is important in bacterial evolution and could be relevant to the somatic mutations that give rise to cancers in multicellular organisms.”
You misread my comment.
I knew exactly what you had meant in your initial comment. I copy-pasted those two paragraphs from the paper to support what I said just prior to those quotations. Thats why I highlighted “induced via the derepression of genes” using bold and did not highlight “unavoidable errors”. Because I knew that the authors were speaking about errors that occur during genome replication. If you have doubt, go through my reply again and see which texts I have highlighted. They were meant to support what I said in this para👇
Right.
I see.
I should have replied the following link (Somatic Hypermutation - Search Results - PubMed) instead of the one I actually gave.
Just kidding😊
Can you read the rest of my post please? Can you show some sign of grasping the concept of an error-prone polymerase? That we are dealing with differences in RATES, and that the nature of the cause of why the rates changed is not relevant to whether the mutations that result under conditions of increased rate do not make them any less random. There’s just more of them being produced.
If you put a gun to my head and tell me to throw dice all day, you essentially “de-repress” my normal dice-throwing habits and massively increase them. The dice I throw are no less random because of it.
Do you understand?
So what? Did I argue that the variations generated by built-in cellular mechanisms are necessarily non-random w.r.t fitness?
The first mechanism I listed in my initial post was meiotic recombination. Right under that topic, I wrote:
After a few para, I wrote:
Variations generated by these mechanisms may or may not end up contributing to adaptive evolution. However, evolution mediated by built-in cellular mechanisms have significant advantages over the traditional mechanism of accidental mutations plus fixation. I’ve provided the references supporting this. (see my reply I gave to Rumraket a day before)
Evolution mediated by built-in cellular mechanisms IS accidental mutation plus fixation.
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Then what in the world do you think random means in random mutations?
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Repeating nonsense is not agreeing to definitions. Comment removed.
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So when a previously functionless sequence of junk DNA undergoes random mutations that confer function upon it (as has been demonstrated to happen), this is an example of undirected evolutionary processes producing Specified Information. Correct?
Origins of New Genes and Pseudogenes | Learn Science at Scitable (nature.com)
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They don’t teach that they are random with respect to location, direction, or frequency. They might oversimplify, but the data (which you completely ignore in favor of words) ONLY show that they are random with respect to FITNESS.
This is objectively false. Please stop with these misrepresentations. If you disagree, provide authors and verbatim quotes.
The “genetic code” is only the mapping of codons to amino acids, not the genome:
The fact that you are misrepresenting it as the latter suggests either mendacity, a lack of basic understanding of biology, or both.
You keep disagreeing with us, so yes.
…that produces changes that are random wrt fitness.
Virtually all of them do not disrupt the genetic code in any way at all. Dude, you don’t even know what “genetic code” means! How about learning more BEFORE pontificating?
They are random wrt fitness.
It does, but the mutations are still random wrt fitness, the only relevant type of randomness.
See my initial reply to you:
Is there something unclear about what I wrote?
Start with your ridiculous misuse of “genetic code.” It’s pretty basic.
“Code” here is metaphorical. True codes involve abstractions that don’t exist in biology.
That’s quite an elision. “Function” is not synonymous with “specification.”
Win my game, or drop this nonsense.
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