Alan Kleinman
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Not when it comes to giving a mathematical explanation of the Kishony and Lenski experiments.
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Not when it comes to giving a mathematical explanation of the Kishony and Lenski experiments.Given my current profession, I think I'm covered.
Not when it comes to giving a mathematical explanation of the Kishony and Lenski experiments.
You avoided the question creationist.I've only seen one real example of a frameshift mutation that didn't completely change the protein coded for. It was an HIV mutant that had a frameshift mutation near the end of the coding sequence and only changed a few amino acids. But if you think that frameshift mutations are the way reptiles evolve into birds and fish evolve into mammals, oh well.
If you mean mutations occur, that's correct. This is taken into account with the absolute fitness of the particular variant as measured by the total number of replications of that variant. But I'm not computing a value of "information", I'm computing the probability of an adaptive mutation occurring which results in an increase in absolute fitness. If you are interested, here's the math:@Alan Kleinman;
I haven't yet read the two papers you refer to, so please excuse me if this is already covered, but I have some issues/questions which aren't immediately obvious from your commentaries on the information models.
i) The first is that the information sequences passed onto offspring are not all conserved ..
How is this taken into account in the calculations of subsequent generation information 'measures'?
If you think that autocatalysis somehow is related to DNA microevolutionary adaptation, you will have to explain that.ii) My second comment is along similar lines, in that (from your descriptions), this model doesn't seem to take into account the principles of autocatalysis, in as far as there is other relevant information to consider with each successive generation. We aren't dealing with a closed system here, y'know(?)
At this point, I have to ask oh wise one, what do you mean by fixation and probably also population as well because apparently we are not speaking the same language?If you actually understood microevolutionary adaptation you would recognize a blunder in the mathematics of the Weinreich paper. Fixation is not required for microevolutionary adaptation, the Kishony experiment demonstrates that. Are all you macroevolutionists this ignorant of microevolutionary adaptation?
Don't expect a macroevolutionist to explain how to compute the probability of at least one instance of a particular mutation occurring as a function of the number of replications of a particular variant.
Please quit proving that you do not know how to use math.So, where is the mathematical explanation of the Kishony and Lenski experiments in your "reliable" journals? And I think you will find that the editors and peer reviewers of "Statistics in Medicine" are not only reliable able to understand the mathematics of microevolutionary adaptation. Only macroevolutionists try to refute this math, sadly they don't have their own explanation other than algae forming colonies and transposon as the way reptiles evolve into birds and fish evolve into mammals.
I'm also unable to see how that answers my question...You are good a seeing the similarities but unable to see the differences.
This is your ultimate problem, you are assuming the chain of being model of only one path forward and this is specifically not how evolution works. single selection pressure environments is not how evolution happens. In fact your own examples are those that are designed to lead to extinction, and we and life are still here so your model as it relates to macroevolution is useless.All you need is a single selection pressure environment with a billion replications for each adaptation step and there you go, reptiles evolving into birds and fish evolving into mammals. So, what do you think the selection pressure is that would do this?
.. but ignores other factors which may/may not affect that specific replication measure(?)If you mean mutations occur, that's correct. This is taken into account with the absolute fitness of the particular variant as measured by the total number of replications of that variant.
So the model deliberately excludes all other factors which might affect that same fitness measure(?)Alan Kleinman said:But I'm not computing a value of "information", I'm computing the probability of an adaptive mutation occurring which results in an increase in absolute fitness. If you are interested, here's the math:
Thanks. Will have a closer look at that .. (so as to be better informed).Alan Kleinman said:The basic science and mathematics of random mutation and natural selection
Sure .. template based replication is likely to have emerged from autocatalysis, but that doesn't mean that the autocatalytic process, and its informational impacts on the replication processes, disappeared altogether.Alan Kleinman said:If you think that autocatalysis somehow is related to DNA microevolutionary adaptation, you will have to explain that.
Yes also, way back, @Alan Kleinman said something like that the purpose of DNA was to self-replicate. (It was unclear whether it was his position, Lenski's, or someone elses?)This is your ultimate problem, you are assuming the chain of being model of only one path forward and this is specifically not how evolution works. single selection pressure environments is not how evolution happens. In fact your own examples are those that are designed to lead to extinction, and we and life are still here so your model as it relates to macroevolution is useless.
Fixation is an end result of evolutionary competition, Darwin called this the "struggle for existence", some people call it survival of the fittest. This is a different physical and mathematical process from DNA microevolutionary adaptation. This is why I continually tell you and the rest of the macroevolutionists to study and understand the differences between the Kishony and Lenski experiments. The Kishony experiment is performed in a large carrying capacity environment that causes minimal competition so that fixation is not required for microevolutionary adaptation to occur. On the other hand, the Lenski experiment is carried on in a much smaller carrying capacity environment which forces competition and fixation to occur in order for microevolutionary adaptation to occur.At this point, I have to ask oh wise one, what do you mean by fixation and probably also population as well because apparently we are not speaking the same language?
That is generally associated with Richard Dawkins "Selfish Gene" which is a simplistic popular piece to introduce a general audience to the subject. That said, add the hammer nail idiom and here we are.Yes also, way back, @Alan Kleinman said something like that the purpose of DNA was to self-replicate. (It was unclear whether it was his position, Lenski's, or someone elses?)
The probability of an adaptive mutation occurring depends only on the beneficial mutation rate and the number of replications of the variant that would benefit from that mutation. Certainly, there are many environmental factors, competition, etc. that would affect that variant from accumulating the replications but that simply means that variant cannot improve fitness under these circumstances.. but ignores other factors which may/may not affect that specific replication measure(?)
(That's only a question not an assertion).
No, I take into account if multiple selection pressures are acting simultaneously, you can read how to do that math here:So the model deliberately excludes all other factors which might affect that same fitness measure(?)
The models I've present aren't for computing information, they compute the probability of a microevolutionary adaptive process occurring.Sure .. template based replication is likely to have emerged from autocatalysis, but that doesn't mean that the autocatalytic process, and its informational impacts on the replication processes, disappeared altogether.
These information models appear as being (intentionally) 'toy' models(?)
Darwin has been dead for a long time, Survival of the fittest was pop term designed to mock Darwin's position much like the Hoyle and the Big Bang and so forth.Fixation is an end result of evolutionary competition, Darwin called this the "struggle for existence", some people call it survival of the fittest. This is a different physical and mathematical process from DNA microevolutionary adaptation. This is why I continually tell you and the rest of the macroevolutionists to study and understand the differences between the Kishony and Lenski experiments. The Kishony experiment is performed in a large carrying capacity environment that causes minimal competition so that fixation is not required for microevolutionary adaptation to occur. On the other hand, the Lenski experiment is carried on in a much smaller carrying capacity environment which forces competition and fixation to occur in order for microevolutionary adaptation to occur.
I never make this assumption. The math I've presented applies to any evolutionary trajectory of microevolutionary adaptation.This is your ultimate problem, you are assuming the chain of being model of only one path forward and this is specifically not how evolution works. single selection pressure environments is not how evolution happens. In fact your own examples are those that are designed to lead to extinction, and we and life are still here so your model as it relates to macroevolution is useless.
I've never said anything like that. It requires the DNA replicase system to replicate DNA.Yes also, way back, @Alan Kleinman said something like that the purpose of DNA was to self-replicate. (It was unclear whether it was his position, or Lenski's?)
Fixation (population genetics) - WikipediaDarwin has been dead for a long time, Survival of the fittest was pop term designed to mock Darwin's position much like the Hoyle and the Big Bang and so forth.
This doesn't seem to have anything to do with fixation as I understand the term, but it might have something to do with the idea of stasis a la the coelacanth. Please try again?
In population genetics, fixation is the change in a gene pool from a situation where there exists at least two variants of a particular gene (allele) in a given population to a situation where only one of the alleles remains.
a 19th-century concept of human society, inspired by the principle of natural selection, postulating that those who are eliminated in the struggle for existence are the unfit.
Darwin is correct, he is describing evolutionary competition and adaptation. He just didn't do the math, he had no idea of DNA.Darwin said:For it should be remembered that the competition will generally be most severe between those forms which are most nearly related to each other in habits, constitution and structure. Hence all the intermediate forms between the earlier and later states, that is between the less and more improved state of a species, as well as the original parent-species itself, will generally tend to become extinct. So it probably will be with many whole collateral lines of descent, which will be conquered by later and improved lines of descent. If, however, the modified offspring of a species get into some distinct country, or become quickly adapted to some quite new station, in which child and parent do not come into competition, both may continue to exist.
It sure looks like that is what you have been doing. Your own posts and language have indicated that in the past.I never make this assumption. The math I've presented applies to any evolutionary trajectory of microevolutionary adaptation.
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