What was the role of organism’s physiology in those examples of molecular evolution? Active or passive?
They are not. For instance, refer the first study. The antibiotic conferring mutations were generated by the derepression of SOS-controlled error prone polymerases. In cell’s point of view, the mutations were not accidental. Instead, the cellular physiology had an active role in generating them. Accidental mutations, in contrast, are unintended disruptions. For eg, when organisms are exposed to certain environmental factors such as ionizing radiations or certain chemical substances. The role of organism’s physiology in evolution is simply passive in the later case.
Consider another example: Meiotic recombination. New alleles produced may be random w.r.t fitness and they may not get fixed in the population. However, what distinguishes them from accidental variations is that the organism’s physiology has an active role in generating the new allele combinations. Its a programmed and regulated process that occurs in the prophase stage of meiosis 1.
“Let us develop the concept of nonrandom mutation here carefully from square one. By “nonrandom mutation” we will mean that the mutation that drives evolution is not accidental—it is not an unintended disruption of the genetic code, caused for example by external agents or by oxidative stress (although mutations of such kinds do happen and can lead to disease). We will take this to mean that the mutation that drives evolution is the result of an organic process that belongs to the organism.”
(Interaction-based evolution: how natural selection and nonrandom mutation work together | Biology Direct | Full Text)
It’s true that technically speaking, the term “genetic code” is not the best choice to use in this context. I could have simply said “genetic sequence” to avoid this confusion.
If you have relevant expertise in a subject area related to this discussion, please flag nonsense comments as Off-Topic so I can remove them.
If you wish to discuss the nonsense, that’s OK too.
Did you ask it?
In all seriousness, the mutations produced by SOS-associated polymerases are just as accidental as those produced by the polymerases normally employed during replication. The “normal” polymerases are activated as part of the cell cycle when it comes time to replicate the genome prior to cell division. These polymerases are no less “induced” by gene expression than the more error-prone polymerases of the SOS response. They just have lower rates of “accidents” than those of the SOS response. The mutations they produce are both random.
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@Midhun: It is challenging to keep any interest in discussing this with you because you do not seem interested in thinking about what others are saying, or thinking about what terms or words mean. When I read your responses I get this sense that you’re in a sort of “I just need to respond” mode, instead of really trying to understand what we are trying to explain to you.
From my perspective I believe I have responded to you in ways that get at the heart of what it means to say a mutation is random, and the relationship between the causes of mutation (what “made” them occur). The responses you have given back seems to just repeat points that, to the best of my ability, I have already explained why fail.
To see an example consider that this part of my previous responses is ignored by you:
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Please define how you are using the terms “physiology,” “active”, and “passive” in that question.
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So what? They are still random wrt fitness, the ONLY way in which mutations are random.
So what? They are still random wrt fitness, the ONLY way in which mutations are random.
I know; I’m a geneticist. They are still random wrt fitness, the ONLY way in which mutations are random.
You’re not addressing that point at all, just beating on a silly straw man.
Ridiculous. Your original claim was:
Your quote is not from a popular book on evolution or a college textbook. Are you implicitly admitting that your claim is false?
No, that would be almost as bad. The correct term is “genome.” Your stubborn, repeated misrepresentation of the most basic terms and concepts shows the shallowness of your data-free approach.
It didn’t confuse me; it was a clear indication that you don’t know what you are talking about. The confused one here is you.
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That’s a polymerase that makes more accidental mutations.
Sure they are. At best, you could claim that the purpose of the change in gene expression is to produce more accidents. No polymerase perfectly copies DNA, so it is matter of how many accidents will occur, not if they will occur.
People have active roles in car accidents. A lottery machine has an active role in selecting ping pong balls with numbers on them, and the results are still random.
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I would not recognize Sultan, Maczek, and Walsh, as prominent evolutionary biologists so much as representatives of the extended evolutionary synthesis, which remains a gadfly stream in biology. The assertion that features such as the vertebrate eye cannot be explained by selection of random genetic mutations certainly is unjustified. I am not a biologist, but I have not found the argument that variation plus natural selection to be fundamentally inadequate, to be very convincing.
You also quote the paper, Interaction-based evolution: how natural selection and nonrandom mutation work together, authored by extended synthesis advocate Adi Livnat. Did you see his paper published last week?
Evolutionary honing in and mutational replacement: how long-term directed mutational responses to specific environmental pressures are possible
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I see no valid reason to doubt the credibility of their papers.
You forgot to say “per se”. It could change the meaning greatly.
Thanks for notifying. Its actually a very long and technical one. I’ll read and comment later.
Why should I address your “still random wrt fitness” arguments when I myself acknowledged the following👇 in my initial post.
It’s evident who is beating the strawman.
Here you go
“Mutations – changes in the genetic sequence of DNA or RNA – are the raw material for evolution.”
(The causes of mutations - Understanding Evolution)
"Mutations are changes in the genetic sequence, and they are a main cause of diversity among organisms."
(http://www.nature.com/scitable/topicpage/genetic-mutation-1127)
"Mutation refers to the actual change in the virus genetic sequence"
(WHO article on SARS-CoV-2)
Happy? Seems like you gonna make me search the whole internet by the time this discussion is over😁
You are trying to downplay the difference. Since you compared “normal” high fidelity polymerase associated with genome replication & SOS-controlled error prone polymerases, let me quote from the first paper:
If you are unwilling to acknowledge this “stark contrast”, I’m sorry dude. I won’t be able to convince you and there is no point in continuing this discussion endlessly. It would be a waste of time for both of us.
Not just the conceptual difference, the evolutionary models that incorporates built-in cellular mechanisms have also got significant advantage over the traditional model. I provided references for that too. Here’s it again👇
The above references show why the following👇downplay of yours is irrelevant. Both may be random. However, one has advantage over other.
Moving On,
No offense, I honestly felt the same.
I haven’t ignored it. Jump to comment 110.
Somewhat like that.
Normal accidents versus staged accidents.
Hi, just a reminder that you haven’t answered this question. Thanks in advance for your reply!
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Yes, yes I am. I am saying that IN EXACTLY THE SENSE THAT MATTERS, the difference is irrelevant. Changing from a LOW to a HIGH rate of mutation does not make those mutations NON-RANDOM no matter what the cause of change in rate is. They’re still random WHEN and IF the system has no way of knowing where mutations of benefit will occur, and are only produced reliably through the fact that A LOT of them occur. Since the MAJORITY do not give any adaptive benefit, it still takes LOTS of random guessing to find the combinations that give adaptive benefit.
No amount of the sentence “in stark contrast” from the paper has any impact on this fundamental point.
I am in fact unwilling to acknowledge that it is relevant for reasons just explained in a perfectly comprehensible way.
The point I am trying to get you to understand is the RANDOMNESS of the mutations themselves. The cause of changes in internal regulation that increases the RATE of mutation is irrelevant with respect to whether they are random or not.
Both may be random? May be? Well they are. And if you admit to that, then you’re now contradicting yourself when you wrote the OP purporting to have found evidence to contradict that it is a fact that:
Yes. Sheer numbers. More random accidents are produced in the short time of the experiment, and thus combinations of mutations that have lower probability of occurring in such a short time interval with the SOS response inactivated, was produced. Notice that it is still a numbers game. Based on probabilities, and that to “beat the odds” then essentially more lottery tickets were bought.
Post 110 did not contain a response to what I wrote here at all:
But since you wrote “they may be random” it seems to have now dawned on you what the whole point is here.
We are not disputing that the cause of the increase in the rate of mutation was due to an induction of a particular regulatory change in gene-expression(initiation of the SOS response). We are disputing your apparent misapprehension that this means the mutations produced aren’t “random accidents” just because they’re the result of error-prone polymerases from the SOS-response. They still very much are.
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Do any of the built-in cellular mechanisms contribute to the evolution of ‘junk’ sequence to functional sequence?
I don’t know what you could be referring to, nor why you are asking the question. Do you think there are tiny “intelligent designers” running around in the gametes of fruit flies, creating functional genes out of junk DNA?
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No-one has done that. Instead, @RonSewell and I have doubted your claim that Sultan et al are “prominent evolutionary biologists” - a claim that you have not retracted even though you know that two of them aren’t even biologists.
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