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What are the limits of Random Variation? A simple evaluation of the probabilistic resources of our biological world

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Coming from a long and detailed discussion about the limits of Natural Selection, here:

I realized that some attention could be given to the other great protagonist of the neo-darwinian algorithm: Random Variation (RV).

For the sake of clarity, as usual, I will try to give explicit definitions in advance.

Let’s call RV event any random event that, in the course of Natural History, acts on an existing organism at the genetic level, so that the genome of that individual organism changes in its descendants.

That’s more or less the same as the neo-darwinian concept of descent with modifications.

A few important clarifications:

a) I use the term variation instead of mutation because I want to include in the definition all possible kinds of variation, not only single point mutations.

b) Random here means essentially that the mechanisms that cause the variation are in no way related to function, whatever it is: IOWs, the function that may arise or not arise as a result of the variation is in no way related to the mechanism that effects the change, but only to the specific configuration which arises randomly from that mechanism.

In all the present discussion we will not consider how NS can change the RV scenario: I have discussed that in great detail in the quoted previous thread, and those who are interested in that aspect can refer to it. In brief, I will remind here that NS does not act on the sequences themselves (IOWs the functional information), but, if and when and in the measure that it can act, it acts by modifyng the probabilistic resources.

So, an important concept is that:

All new functional information that may arise by the neo-darwinian mechanism is the result of RV.

Examining the Summers paper about chloroquine resistance:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4035986/

I have argued in the old thread that the whole process of generation of the resistance in natural strains can be divided into two steps:

a) The appearance of an initial new state which confers the initial resistance. In our example, that corresponds to the appearance of one of two possible resistant states, both of which require two neutral mutations. IOWs, this initial step is the result of mere RV, and NS has no role in that. Of course, the initial resistant state, once reached, can be selected. We have also seen that the initial state of two mutations is probably the critical step in the whole process, in terms of time required.

b) From that point on, a few individual steps of one single mutation, each of them conferring greater resistance, can optimize the function rather easily.

Now, point a) is exactly what we are discussing in this new thread.

So, what are the realistic powers of mere RV in the biological world, in terms of functional information? What can it really achieve?

Another way to ask the same question is: how functionally complex can the initial state that for the first time implements a new function be, arising from mere RV?

And now, let’s define the probabilistic resources.

Let’s call probabilistic resources, in a system where random events take place, the total number of different states that can be reached by RV events in a certain window of time.

In a system where two dies are tossed each minute, and the numbers deriving from each toss are the states we are interested in, the probabilistic resources of the system in one day amount to  1440 states.

The greater the probabilstic resources, the easier it is to find some specific state, which has some specific probability to be found in one random attempt.

So, what are the states generated by RV? They are, very simply, all different genomes that arise in any individual of any species by RV events, or if you prefer by descent with modification.

Please note that we are referring here to heritable variation only, we are not interested to somatic genetic variation, which is not transmitted to descendants.

So, what are the probabilistic resources in our biological world? How can they be estimated?

I will use here a top-down method. So, I will not rely on empirical data like those from Summers or Behe or others, but only on what is known about the biological world and natural history.

The biological probabilstic resources derive from reproduction: each reproduction event is a new state reached, if its genetic information is different from the previous state. So, the total numbet of states reached in a system in a certain window of time is simply the total number of reproduction events where the genetic information changes. IOWs, where some RV event takes place.

Those resources depend essentially on three main components:

  1. The population size
  2. The number of reproductions of each individual (the reproduction rate) in a certain time
  3. The time window

So, I have tried to compute the total probabilistic resources (total number of different states) for some different biological populations, in different time windows, appropriate for the specific population (IOWs, for each population, from the approximate time of its appearance up to now). As usual, I have expressed the final results in bits (log2 of the total number).

Here are the results:

 

Population Size Reproduction rate (per day) Mutation rate Time window Time (in days) Number of states Bits + 5 sigma Specific AAs
Bacteria 5.00E+30 24 0.003 4 billion years 1.46E+12 5.26E+41 138.6 160.3 37
Fungi 1.00E+27 24 0.003 2 billion years 7.3E+11 5.26E+37 125.3 147.0 34
Insects 1.00E+19 0.2 0.06 500 million years 1.825E+11 2.19E+28 94.1 115.8 27
Fish 4E+12 0.1 5 400 million years 1.46E+11 2.92E+23 78.0 99.7 23
Hominidae 5.00E+09 0.000136986 100 15 million years 5.48E+09 3.75E+17 58.4 80.1 19

The mutation rate is expressed as mutations per genome per reproduction.

This is only a tentative estimate, and of course a gross one. I have tried to get the best reasonable values from the sources I could find, but of course many values could be somewhat different, and sometimes it was really difficult to find any good reference, and I just had to make an educated guess. Of course, I will be happy to acknowledge any suggestion or correction based on good sources.

But, even if we consider all those uncertainties, I would say that these numbers do tell us something very interesting.

First of all, the highest probabilistic resources are found in bacteria, as expected: this is due mainly to the huge population size and high reproduction rate. The number for fungi are almost comparable, although significantly lower.

So, the first important conclusion is that, in these two basic classes of organisms, the probabilistic resources, with this hugely optimistic estimate, are still under 140 bits.

The penultimate column just adds 21.7 bits (the margin for 5 sigma safety for inferences about fundamental issues in physics). What does that mean?

It means, for example, that any sequence with 160 bits of functional information is, by far, beyond any reasonable probability of being the result of RV in the system of all bacteria in 4 billion years of natural history, even with the most optimistic assumptions.

The last column gives the number of specific AAs that corrispond to the bit value in the penultimate column (based on a maximum information value of 4.32 bits per AA).

For bacteria, that corresponds to 37 specific AAs.

IOWs, a sequence of 37 specific AAs is already well beyond the probabilistic resources of the whole population of bacteria in the whole world reproducing for 4 billion years!

For fungi, 147 bits and 34 AAs are the upper limit.

Of course, values become lower for the other classes. Insects still perform reasonably well, with 116 bits and 27 AAs. Fish and Hominidae have even lower values.

We can notice that Hominidae gain something in the mutation rate, which as known is higher, and that I have considered here at 100 new mutations per genome per reproduction (a reasonable estimate for homo sapiens). Moreover, I have considered here a very generous population of 5 billion individuals, again taking a recent value for homo sapiens. These are  not realistic choices, but again generous ones, just to make my darwinist friends happy.

Another consideration: I have given here total populations (or at least generous estimates for them), and not effective population sizes. Again, the idea is to give the highest chances to the neo-darwinian algorithm.

So, these are very simple numbers, and they should give an idea of what I would call the upper threshold of what mere RV can do, estimated by a top down reasoning, and with extremely generous assumptions.

Another important conclusion is the following:

All the components of the probabilistic resources have a linear relationship with the total number of states.

That is true for population size, for reproduction rate, mutation rate and time.

For example, everyone can see that the different time windows, ranging from 4 billion years to 15 million years, which seems a very big difference, correspond to only 3 orders of magnitude in the total number of states. Indeed, the highest variations are probably in population size.

However, the complexity of a sequence, in terms of necessary AA sites, has an exponential relationship with the functional information in bits: a range from 19 to 37 AAs (only 18 AAs) corresponds to a range of 24 orders of magnitude in the distribution of probabilistic resources.

Can I remind here briefly, without any further comments, that in my OP here:

I have analyzed the informational jump in human conserved information at the apperance of vertebrates? One important result is that 10% of all human proteins (about 2000) have an information jump from pre-vertebrates to vertenrates of at least (about) 500 bits (corresponding to about 116 AAs)!

Now, some important final considerations:

  1. I am making no special inferences here, and I am drawing no special conclusions. I don’t think it is really necessary. The numbers speak for themselves.
  2. I will be happy of any suggestion, correction, or comment. Especially if based on facts or reasonable arguments. The discussion is open.
  3. Again, this is about mere RV. This is about the neutral case. NS has nothing to do with these numbers.
  4. For those interested in a discussion about the possible role of NS, I can suggest the thread linked at the beginning of this OP.
  5. I will be happy to answer any question about NS too, of course, but I would be even more happy if someone tried to answer my two questions challenge, given at post #103 of the other thread, and that nobody has answered yet. I paste it here for the convenience of all:

Will anyone on the other side answer the following two simple questions?

1) Is there any conceptual reason why we should believe that complex protein functions can be deconstructed into simpler, naturally selectable steps? That such a ladder exists, in general, or even in specific cases?

2) Is there any evidence from facts that supports the hypothesis that complex protein functions can be deconstructed into simpler, naturally selectable steps? That such a ladder exists, in general, or even in specific cases?

Comments
Corey Delvine: "p = q implies that q = p" Are you serious? Are you confounding logical implication with identity? Sometimes you amaze me! :) So, for you: "If p then q" is the same as p = q Good to know...gpuccio
November 15, 2017
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Corey Delvine: "This is where gpuccio assumes that only this conserved sequence represents the only functional sequence of said protein. Do I have to spell it out for you? This is where Gpuccio is implying that function = conserved sequence homology." Not at all. I only assume that conservation is a very good way of measuring how much that sequence cannot change, how much it is functionally constrained. I am not saying that it is the only functional sequence. I am saying that the Blast bitscore is a good measure (probably an underestimate) of the functional information in the protein. Please, read my post #70. I paste here the relevant part, for your convenience:
But let’s go back to an old friend, ATP synthase. As I have said many times, the beta chain in the F1 complex of the molecule has an astonishing conservation between bacteria and humans. Just to remind the numbers (humans and E. coli): ATP synthase beta chain (P06576, 553 AAs): 334 identities, 383 positives, 663 bits Now, that is amazing. Consider that this result in bits is already a measure of the target space/search space ratio. Indeed, the search space for this proteins is 2390 bits, about 10^719 states. Therefore, when we have 663 bits of functional information from the bitscore, that is already a very conservative value, because it is setting the target space at 1727 bits, IOWs a target space of 10^519 states! IMO, the blast bitscore is definitely underevaluating functional information. For example, it gives perfect identity a botsocre of about 2.2, which is half the potential information in one AA position (4.3 bits). That derives in part from how the bitscore is computed, but I still believe that it underevaluates functional information. Hoever, as it is a measure that is very easy to obtain, and is universally considered a valid metrics of homology, I have used that score in all my analyses. But my point is that the bitscore is already corrected, maybe hypercorrected, for the target space.
I would not say that estimating a target space of 10^519 is the same as saying that "this conserved sequence represents the only functional sequence of said protein". There are 519 orders of magnitude of difference between the two statements!gpuccio
November 15, 2017
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Mung: Yes, I was afraid that I was making undue advertising! :)gpuccio
November 15, 2017
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Origenes: "I don’t think that GPuccio is very concerned with the question if the function is the same or not. Please GPuccio, correct me if I am wrong. But, why would that be relevant? It is enough to know that it is functional, based on being conserved for long evolutionary times. The main point of blasting, as I understand it, is that we can see the evolutionary history of the functional sequence." Correct. But, of course, in the case of known proteins or known domains, it is easy to see that the function is more or less the same. That is not easy when we find conservation of sequences whose function is not known, as I have often done.gpuccio
November 15, 2017
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gpuccio:
The chosen AAs are IKEA and G.
Must be a Swedish team.Mung
November 15, 2017
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You cannot draw the conclusion that the function also "jumped" into existence solely based on the appearance of a certain amino acid sequence. This is where gpuccio assumes that only this conserved sequence represents the only functional sequence of said protein. Do I have to spell it out for you? This is where Gpuccio is implying that function = conserved sequence homology. And this is completely incorrect.Corey Delvine
November 15, 2017
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Corey Delvine:
I’m just doing my part to push back, no matter how futile.
Perhaps change your username to Sisyphus.Mung
November 15, 2017
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To all interested: Let's remind Corey' statement: "experiments have swapped amino acids in proteins, heck they’ve even stripped all 20 amino acids away and rebuilt proteins using only 4 amino acids and the protein was still functional" 1) We have already found a first important error: exchanging a protein domain for a protein. 2) Corey has graciously anticipated another small and obvious error: it's not 4 AAs, but 5. Not so important. 3) Let's go to the statement that the protein, I beg your pardon the protein domain, was "stripped away of all 20 amino acids and rebuilt". Is that true? No. The aim of the experiment is to simplify the sequence according to a 5 AAs alphabet. The chosen AAs are I,K,E,A and G. But, as the authors say, simplification was attempted only in the "residues not implied in binding", IOWs in the residues not directly implied in the function of the domain. IOWs, the most important residues from the point of view of function. How many are the residues where simplification was simply not attempted? They are 12. Let's go to Fig. 2b, which shows the sequence of the two "functional" (more on that later) simplified domains that were the final result of the whole process, as compared to the sequence of the wildtype. residues (from left): 6,7,8,15,33,34,35,47,49,50,51,52 12 AAs (21% of the molecule) were left as in the wild type, IOWs as they were from an alphabet of 20 AAs! But there is more. Of the 45 AAs were the simplification was attempted, it was achieved (in the final "functional" two sequences) only in 40 out of 45 residues, the authors say. Indeed, they say something slightly different, and we will see the reason for that. It's a real trick they are trying, so be very careful. What they say is: "In the more simplified variant, FP2" (IOWs their best result) "40 of the 45 residues at which simplification was attempted are I,K,E,A or G." Strange way to say it. But there is a reason for that. A reason that is a subtle deception. But for the moment, let's acknowledge this simple truth: the simplification failed in 5 residues where it was attempted. But in the Figure I can find only 4 of them. Residues 2,16,17,42 The fifth residue in black, the S at 50, is indeed one of the 12 AAs mentioned before, So, there must be some error in the paper. OK, not important. Let's say that in FP2 simplification failed in 4 residues. That makes: 12 + 4 = 16 AAs, 28% of the sequence which has not been simplified at all. But there is more. Here comes the trick, the deception. The authors say: ""In the more simplified variant, FP2" (IOWs their best result) "40 of the 45 residues at which simplification was attempted are I,K,E,A or G." So, it would seem that 40 (or 41) of the residues have been "simplified", isn't it? But that's not the case. If you look at the sequence of FP2, you will see that 13 residues: Residues 4,19,20,21,22,26,31,32,37,43,46,48,54 were already IKEA or G in the wild type, and that they have not changed in FP2. Not at all. IOWs, they have not been "simplified" at all, they have remained the same, and they were alredy from the 5 chosen AAs in from the beginning. Coming, of course, from an alphabet of 20 AAs. Can you see the subtle deception? So, let's see. We have: 12 + 4 + 13 = 29 AAs (50.9% of the whole sequence) where no simplification has been accomplished at all. So, is Corey's statement that: "heck they’ve even stripped all 20 amino acids away and rebuilt proteins using only 4 amino acids" accurate? Is that even close to truth? Of course not. Another big, big error. But I must admit that here it's not all Corey's fault. He should have noticed that in 12 important AAs no simplification was even attempted, because that is clearly stated by the authors. So, he's responsible for that error. He should have noticed that in 4 or 5 AAs the simplification simply did not work, because that is clearly stated by the authors. So, he's responsible for that error. But he is not fully responsible for not noticing that 13 AAs had not changed from the wildtype, because they were already AAs included in the chosen 5 from the beginning. The authors do not say that clearly. Indeed, it seems that they try to hide that important fact. So, third big error. They are already a lot, aren't they, Corey? I have still much to say about SH3 and the paper, and other papers on the subject. Maybe I will not find other big errors from Corey, but probably some imprecision that deserves clarification. But that will have to wait until tomorrow. :)gpuccio
November 15, 2017
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Corey Delvin @229
GPuccio: “My entire argument depends on this: sequence homology (conserved for long evolutionary times) = function Not the other way round.”
Corey Delvin: The first part of your argument depends on sequence homology (conserved for long evolutionary times) = function.
Indeed, when a sequence is conserved for long evolutionary times, we can safely infer that this particular sequence has biological function. BTW this means we do not have to know which specific function, in order to know that it has function.
Corey: When you blast a human protein to another organism and infer that very high homology suggests the same function. And I’m fine with that.
I don’t think that GPuccio is very concerned with the question if the function is the same or not. Please GPuccio, correct me if I am wrong. But, why would that be relevant? It is enough to know that it is functional, based on being conserved for long evolutionary times. The main point of blasting, as I understand it, is that we can see the evolutionary history of the functional sequence.
Corey: But the second you start making calculations about sequence space based on conservation of sequence homology and conclude that the jump in homology coincides with a rapid evolution of function …
If we see the sudden addition of 1000’s bits followed by extreme conservation of the new sequence, what other conclusion can be drawn?
Corey: … you are implying that function = conserved homology.
Not at all. We see that the new sequence is conserved for long evolutionary times and from this we infer that it is a (new) functional sequence. There is no reason whatsoever to have it backwards. - - - Corey Delvin @236 You cannot provide one single quote by GPuccio that supports your idiotic claim.Origenes
November 15, 2017
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Warped? It is an exact summary of how the previous conversation went. You're now in the same troll-boat as ET, Dio, and MungyCorey Delvine
November 15, 2017
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Corey Delvin @232
Origenes: You cannot provide one single quote by GPuccio that supports your absurd claim.
Corey Delvin: Did you not read the rest of #227, Origenes?
I did. You are not quoting GPuccio. All you offer is your warped view of his argument.Origenes
November 15, 2017
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p = q implies that q = p don't obfuscateCorey Delvine
November 15, 2017
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Corey Delvine: p-->q does not imply that q-->p. And now, let's go to the paper.gpuccio
November 15, 2017
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Did you not read the rest of #227, Origenes?Corey Delvine
November 15, 2017
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Corey Delvine: "This is all evident in his apparent belief that evolution has to find a “specific” sequence in order to get function, which is, again, completely wrong." Whether a specific function is coded with homologous or non-homologous sequences is completely unrelated to the ratio between target space and search space for the environment where this function is beneficial. If these non-homologous sequences: TTT, CGC and ACA are functional in a specific environment(target space of size 3), the ratio (3/4^3) would not change if those sequences were homologous - for e.g. AAA, AAC, AAT. Your assertion is therefore beside the point.forexhr
November 15, 2017
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Corey Delvin @227
Origenes: Corey Delvin is a guy who believes that natural selection in the lab requires building “an entire ecosystem and monitor every single aspect for millions of years. ... it is simply stupid beyond belief.
Corey Delvin: No, that is what Gpuccio requires.
You are absolutely wrong. 100%. You cannot provide one single quote by GPuccio that supports your absurd claim.Origenes
November 15, 2017
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"My entire argument depends on this: sequence homology (conserved for long evolutionary times) = function Not the other way round." You don't even understand your own argument. The first part of your argument depends on sequence homology (conserved for long evolutionary times) = function. When you blast a human protein to another organism and infer that very high homology suggests the same function. And I'm fine with that. But the second you start making calculations about sequence space based on conservation of sequence homology and conclude that the jump in homology coincides with a rapid evolution of function, you are implying that function = conserved homology. Which, it does not.Corey Delvine
November 15, 2017
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Mung @203: "Could have predicted the insults were coming." It should have been obvious given the lack of serious arguments by the dissenting commenter. Running out of arguments leads some folks -unwilling to search for the truth- to insulting their opponents. Nothing new. It's been that way since the beginning of history.Dionisio
November 15, 2017
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'Corey Delvin is a guy who believes that natural selection in the lab requires building “an entire ecosystem and monitor every single aspect for millions of years”' No, that is what Gpuccio requires. Any experiment on the evolution of protein function, that doesn't support Gpuccio's worldview, he lumps into the category of "artificial selection." His reasoning is that (in his opinion) the experiment did not do a good enough job demonstrating biological relevance. Which of course would be understandable, except for the fact that his requirements for biological relevance are absurd: It has to be in a living organism, you have to see it increase fitness, etc. Hence, why the only thing he seems to admit is natural selection is a study in viruses. These are all ridiculous requirements when taking into account the complexities of the molecular biology techniques that would be required. To do these experiments on bacterial or eukaryotic proteins, things must be simplified.Corey Delvine
November 15, 2017
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Corey D:
In my world, the word protein refers to any segment of amino acids over 50 residues.
Fine. Now demonstrate that blind and mindless processes can produce one. Or admit that your position is for losers.ET
November 15, 2017
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Corey D:
I do find it disgusting though, how the “science” behind the ID movement preys on the lack of knowledge most people have in the field of biology.
Totally clueless. Evolutionism is alive and well due to lack of knowledge. Nice own goalET
November 15, 2017
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"sequence homology (conserved for long evolutionary times) = function" but function =/= sequence homology (conserved for long evolutionary times) This should tell you there is something inherently (and glaringly) wrong with your approach. Also, that's not how (correct) equations work.Corey Delvine
November 15, 2017
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GPuccio @221 There is this saying:
"Never start a fight with an idiot, he'll only pull you down to his level and beat you with his stupidity."
Origenes
November 15, 2017
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Ah yes, wikipedia trumps all. Now I know with 100% certainty that we are doing "science" And just for you Gpucc, I will restate: Baker rebuilt a protein DOMAIN using just 5 amino acids and it folded properly and remained functional. Protein or protein domain, it does not affect my claims in anyway. But the fact that the function is retained with this highly simplified amino acid repertoire does shred your personal beliefs about sequence space. Of course you will find a way to remain ignorant though.Corey Delvine
November 15, 2017
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Origenes: Thank you. I have the impression that our "friend" is simply trying to prevent me from completing my argument about "his" paper, because I am wasting the few time I have answering his blunder.gpuccio
November 15, 2017
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Corey Delvine: "His entire argument depends on this: function = sequence homology" As usual, you have it all wrong. My entire argument depends on this: sequence homology (conserved for long evolutionary times) = function Not the other way round. Sometimes I really wonder if you really don't understand things, or if you are just doing it for the hell of it! OK, it's not important. You are an occasion to explain important points, and I am grateful to you for the role you play, either unwillingly or intentionally. You say: "This is all evident in his apparent belief that evolution has to find a “specific” sequence in order to get function, which is, again, completely wrong." Evolution certainly has to find a specific sequence that can implement some specific function, for that function to be present. Even a child would understand that. Of course, there is often more than one specific sequence that can implement a function. It's called the target space, and it is one of the basic concepts in ID.gpuccio
November 15, 2017
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Corey Delvin @208
CD: So once again, much like your demand that researchers build an entire ecosystem to demonstrate selectability and therefore function, you are simply being ridiculous.
Here you repeat the blunder you previously made in the thread What are the limits of Natural Selection? A blunder based on a complete misunderstanding of GPuccio's argument concerning artificial selection. Here is my comment again:
… Corey Delvin is a guy who believes that natural selection in the lab requires building “an entire ecosystem and monitor every single aspect for millions of years” (post #228, #232 and #239). This is not at all a joke by Corey, he seriously holds that when you [GPuccio] are talking about artificial selection that you are objecting to the absence of such an ecosystem. That is his genuine understanding of the discussion…. No one has commented on this, because it is simply stupid beyond belief.
Origenes
November 15, 2017
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The basic premise of Gpuccio's argument is based on a lack of knowledge, forexhr. His entire argument depends on this: function = sequence homology But this is false and I have pointed to numerous lines of experimental evidence that show this. This also makes his sequence space calculations completely worthless. This is all evident in his apparent belief that evolution has to find a "specific" sequence in order to get function, which is, again, completely wrong.Corey Delvine
November 15, 2017
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Corey Delvine: "You say that because the 57 amino acid segment is “just” a protein domain, and not a full-length protein, it doesn’t support my claim." It certainly does not support your claim about proteins. Try to formulate again your claim, making it about one short protein domain, and at least that part will be correct. The rest, I still have to deal with.gpuccio
November 15, 2017
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Corey Delvine: "With every word you type, it seems that Gpuucio’s world is more and more different from the real world." It is certainly different from your world. Luckily. "In my world, the word protein refers to any segment of amino acids over 50 residues." From Wikipedia: "Proteins (/?pro??ti?nz/ or /?pro?ti.?nz/) are large biomolecules, or macromolecules, consisting of one or more long chains of amino acid residues". "Many proteins are composed of several protein domains, i.e. segments of a protein that fold into distinct structural units." IOWs, a protein is a molecule, a domain is a segment of a protein, and is not an individual molecule. Your definition for protein: "any segment of amino acids over 50 residues" is simply wrong. Length is useful to distinguish between proteins and peptides, which are both complete molecules: Always from Wikipedia: "The words protein, polypeptide, and peptide are a little ambiguous and can overlap in meaning. Protein is generally used to refer to the complete biological molecule in a stable conformation, whereas peptide is generally reserved for a short amino acid oligomers often lacking a stable three-dimensional structure. However, the boundary between the two is not well defined and usually lies near 20–30 residues.[5] Polypeptide can refer to any single linear chain of amino acids, usually regardless of length, but often implies an absence of a defined conformation." So, peptides are shorter molecules, while proteins are longer molecules, but both are whole molecules. Domains are by definition functional subunits of proteins, they are not whole molecules. In particular, the SH3 domain is part of a lot of much longer proteins. It is not a protein. Always from Wikipedia: "The SRC Homology 3 Domain (or SH3 domain) is a small protein domain of about 60 amino acid residues. Initially, SH3 was described as a conserved sequence in the viral adaptor protein v-Crk. This domain is also present in the molecules of phospholipase and several cytoplasmic tyrosine kinases such as Abl and Src.[1][2] It has also been identified in several other protein families such as: PI3 Kinase, Ras GTPase-activating protein, CDC24 and cdc25.[3][4][5] SH3 domains are found in proteins of signaling pathways regulating the cytoskeleton, the Ras protein, and the Src kinase and many others. " Your world is full of gross errors, but it is also a world where you never admit one. Just a friendly advice: next time, you ask first your biology teacher, if you have one.gpuccio
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