I often encounter posters here at TSZ who claim that Genetic Algorithms (GAs) either model or simulate evolution. They are never quite clear which it is, nor do they say what it means to model or simulate evolution (what would be required) and how GAs qualify as either one or the other. My position is that GAs neither model nor simulate evolution. In addition to other reasons I’ve given in the past I’d like to present the following argument.
GAs are often used to demonstrate “the power of cumulative selection.” Given small population sizes drift ought to dominate yet in GAs drift does not dominate. Why not?
Three questions:
- How do we determine the effective population size for a GA?
- How do we calculate the value of the selection coefficient?
- How do we determine when genetic drift will overcome the effects of selection?
In a GA written by keiths (a version of the WEASEL program) the default population size is 200.
#define POPULATION_SIZE 200 // total population size
Effective population size is the number of individuals in a population who contribute offspring to the next generation.
Even though the population size is 200, only one is selected to contribute offspring to the next generation.
#define NUM_SURVIVORS 1 // number of survivors per generation (must be less than POP_SIZE)
Given an effective population size of one, drift ought to dominate, but it doesn’t.
Given an effective population size of one, what must the selection coefficient be for drift to not dominate selection?
I’d truly appreciate any assistance with the concepts or the math.
In any event, there is no way that this GA (the keiths WEASEL program) either models or simulates evolution.
Reference:
Flint,
New proteins discovered in a lab? Can you elaborate on this discovery. What function could these proteins perform? How many amino acids in the sequence? How would you propose the genome could evolve to go from these proteins to more complex proteins?
What mechanism do you propose that would get these proteins to be transcribed in a timely manner that allowed the cell cycle to remain in control?
Welcome, JoeCoder. Thank you for coming here to defend your forum.
For those not on Reddit, I would like to share the link to your subreddit: http://www.reddit.com/r/creation. When one visits that page, even as a logged in Reddit user, this message is shown:
The referenced rules are:
If you had good arguments and evidence, your relatively small numbers would not matter. If you were genuinely interested in learning whether or not creationism, including the intelligent design variant, is supported by the scientific evidence, you wouldn’t require a purity test before allowing full access. Your rules describe an echo chamber.
Please do let your members know that they are welcome here, with no ideological check required.
Welcome JoeCoder. I think you’re also at UD?
The main problem I have with this statement is, that there are entire enormous libraries of factually supported evidence for a trial and error (with successes retained) process. This evidence has been amassed over the last century and a half, by tens of thousands of researchers, and documented, tiny piece by tiny piece, in tens of thousands of peer-reviewed journal articles.
So as far as I can see, you are like the geocentrist who claims that he’ll agree that the earth circles the sun as soon as some “real science” provides real factual evidence. But pending evidence (that satisfies him), he’ll stick with what he can see with his eyes – that the sun obviously rises and sets, while the earth is stationary. And, of course, the mechanisms for a heliocentric solar system have not been discovered.
What can anyone say to this? All we can do is laugh while backing slowly away…
I am repeating what (I think) DNA_jock said. He is in that profession, and knows what he’s talking about. So please don’t be so hasty to move the goalposts until you have asked exactly what has been accomplished. THEN move the goalposts. Otherwise, you might move them right in front of the kick by mistake.
Do you have any candidates for this “mechanism” that you believe has not yet been discovered? Bonus points if you can define this “mechanism” in sufficient detail, and with sufficient clarity, that’s it’s possible to tell whether or not said “mechanism” has been in operation in any particular case.
Flint,
You are ignoring my questions. I have known about the lab experiments for a long time but they do little to reduce my skepticism. Getting 15 to 20 amino acid poly peptides to do limited enzyme reaction does very little to prove the mechanism that has to build proteins with between 50 and 34000 amino acids. Flint why do you believe this mechanism explains all life’s diversity?
cubist,
I have no idea at this point. I don’t believe the ID guys, Shapiro or anyone else has a good alternative. I believe I don’t know is a better answer then the only alternative you can think of now. Especially given the sequential space of the genome that has to be worked through by random change. This is just my humble opinion. There are many things we still don’t understand in science, I think it was premature to declare understanding once we saw the sequence challenges with DNA.
No, you are moving the goalposts. First you claim that trial and error plus selection can’t produce proteins. When it turns out that no only does this method work, but even in the lab it excels, then you want the protein to do something specific. When it does, and treats a specific illness, THEN you want more amino acids! And if it has as many amino acids as you demand, THEN you want it to be part of the genome! Watch those goalposts fly!
You dismiss a concept because the proof of concept doesn’t meet your standards? Imagine that.
Well, first let’s dismiss the idea that random mutation plus selection explains all life’s diversity. It is one of several mechanisms in operation. For all I know, it may not be the most important. But when it is simulated, the simulations produce what is observed. And the more complex the simulations, the closer the match. This ought to be a hint that we’re on the right track, if you choose to recognize it.
Beyond that, I feel like I have demonstrated the potential of a journey of a thousand miles simply by walking across the room. See, the process works! But no, you simply refuse to grasp that this same process, carried on for a few billion years, can travel immense distances. You’re still stuck in that little room.
To me, if it can be demonstrated that mutation+selection can add a SINGLE amino acid, then the process is established. If you don’t accept this, you are going to have to justify why there is some sort of physical limit at N amino acids, such that the N+1th cannot possibly be added.
The DNA sequence of Homo sapiens contains roughly 3.2 billion nucleotides. Looking at single-nucleotide mutations only, there’s exactly 4 (four) different things that can happen to a single nucleotide in an existing sequence:
One, the nucleotide can be deleted. There being 3.2 billion nucleotides in human DNA, it follows that there are 3.2 billion possible mutations which involve deleting a single nucleotide from human DNA.
Two through four, the nucleotide can be replaced by one of the three nucleotides it isn’t—that is, Adenine could be replaced by Cytosine, or Guanine, or Thymine; Cytosine could be replaced by Adenine, or Guanine, or Thymine; and so on. WIth 3.2 billion nucleotides in human DNA, there are (3.2E9 * 3 =) 9.6 billion possible mutations which involve replacing a single nucleotide in human DNA.
And, still looking at single-nucleotide mutations, a single ‘new’ nucleotide (Adenine, Cytosine, Guanine, or Thymine) can be inserted in between any neighboring pair of nucleotides in the existing sequence. Given 3.2 billion hucleotides in human DNA, there are, therefore, (3.2E9 * 4 =) 12.8 billion possible mutations which involve inserting a single nucleotide into the existing human DNA sequence.
The total number of possible single-nucleotide mutations which can occur in human DNA is, therefore: (3.2E9 + 9.6E9 + 12.8E9 =) 25.6 billion.
As of 2016, there are over 7 billion human beings on Earth.
For any given Single-Nucleotide Mutation X, what is the probability that that mutation exists, and can be found in at least one living member of the human species?
How long will it take the human species to generate a sufficient number of births that every one of those 25.6 billion single-nucleotide mutations can be found in at least one human being?
What does the above do to your apparent conviction that “sequential space” is just too darn big for the identified mechanisms of evolution to work?
colewd,
Random change plus selection.
And if that’s your concern, then please read Arrival of the Fittest by Andreas Wagner. The research he presents shows that the structure of sequence space is very friendly to evolution.
It’s bad news for ID.
Just to be pedantic, the answer is anywhere from a few years to forever, depending. I think what you meant to ask was, IF every possible single-nucleotide mutation is equally probable, how long before the odds of every one occurring exceeds 50%.
Still the wrong question, I think. He’s not asking about specific point mutations, he’s asking about the probability of very long complex sequences, given that (1) long sequences are improbable exponentially to their length; and (2) Very very few of these highly unlikely happenstances are likely to be useful (and selected to fixation).
As WEASEL has demonstrated so ably, the concept of selection just seems incomprehensible to the creationist. The probability of some useful complex protein occurring at random is as far as they get, and the notion that selection changes these odds from essentially impossible to essentially inevitable is just a river a bit too wide to leap across.
Flint,
Here is the main cause of my skepticism. The sequential space of an amino acid with 21 amino acids is 10 times larger then one with 20 so the problem gets 10x worse for every amino acid added. The lab experiments are too small to show the real world problem. I know this will sound strange to you but you are not comparing walking around the room with walking a thousand miles. You are comparing walking around a room with walking to the end of our galaxy if you compare the lab with the smallest human protein insulin. This is why average proteins break trial and error searches. This is why the weasel program needs a target. I have to break now will be on late tomorrow am west coast time.
cubist,
I will be back tomorrow. But again the sequential space of a the total hemoglobin protein in side the genome is 4^1500. I know you realize this is a really big number and the argument is that there are a lot of versions of hemoglobin that can work, but the research I have done says that this is small compared to the total possibilities.
And here is the main problem everyone is having with you. At any given step in the development of a protein, the question is whether ONE added amino acid is beneficial (or not too harmful). And the challenge of adding ONE amino acid is the same no matter how many have already been added.
Not really. You are ignoring selection, and you are ignoring time.
Trial and error PLUS SELECTION. Your omission of this critical factor, over and over and over and over, is symptomatic. I have become convinced that since selection overcomes all the problems you are inventing, you simply cannot SEE the word. Your mind just tunes it right out.
The WEASEL program had a target because the purpose of the program was to illustrate the power of selection, not to simulate evolution. In the real world of biology, the target is whatever works. And the space of whatever works is enormous. The chance of the bullet falling to the ground precisely HERE is infinitesimal. The chances of it falling somewhere are unity.
And it’s the same with your proteins. The chances of those exact proteins evolving is hopelessly tiny. If we were to rerun evolution from scratch we could do it an infinite number of times and never get even close to the same proteins twice. We might have some runs where we get no proteins at all, but some form of life only vaguely analogous.
Except, of course, for SELECTION. Over the course of a billion years, hemoglobin proteins developed one very occasional step at a time, and could have wandered off in some other USEFUL AND SELECTED direction at any time. But each selected step worked well enough to be retained. (and of course, many organisms don’t use anything like hemoglobin.)
Are you arguing Origin of Life, or biological evolution? That looks like a Origin of Life argument. Most people will agree that origin of life is not yet explained.
Yes. And if every last amino acid simply must fall exactly into place at the same time, all of them at once, in one fell swoop, this is a problem.
If, on the other hand, it’s not mandatory that every amino acid fall exactly into place, all of them at once, in one fell swoop…
I tried the “journey of many steps” analogy, and he rejected it as being like “walking across the galaxy.”
Unfortunately, he didn’t specify whether he simply thought the journey to life as we know it is simply too far to be reached (requires too many steps), or whether he thinks one or more qualitatively distinct leaps he can’t describe are required.
Either way, it boils down to “I refuse to believe it, therefore it didn’t happen that way”, which basically stops any conversation.
colewd,
I am sure you believe that is the case, but you are hopelessly mistaken. Most of the people here appear to have actually thought about the theory of evolution, and their provisional assent is based on a more or less careful examination of the data. That your “belief” was changed by the “realization” that “the genome was a mathematical sequence” (a lovely category error) is, as kairosfocus would put it, telling.
Why bother? You claim to have known about these lab experiments “for a long time”. How about you get a tad more specific about their shortcomings?
Binding to pretty much every ligand the researchers tried.
See below…
C-terminal addition, and unequal cross-over
Well, they might be transcribed constitutively, and not interfere with the cell cycle, like, y’know, housekeeping genes…I mean really, WTF?
oh dear, you are betraying your ignorance here 🙂
Oh-err. Szostak technology has been used to develop 50aa polypeptides. Care to move the goalposts again? How about 100aa (although not all random) polypeptides? Interesting, too, that you mention a 34,000aa protein. Thinking of titin perhaps? Have you actually looked at titin? It’s tandem repeats of 80aa and 100aa domains. Think that duplication might have played a role? At all?
Why do you think it cannot? Please be far, far more specific than you have been to date.
What, specifically, is the barrier that you believe prevents a 15-50aa protein from becoming an 80-100aa protein (via duplication, recombination and C-terminal addition), and what prevents a 80-100aa protein from becoming a 34,350aa (well, in mice a 35,213aa) protein? Does this mean that God loves mice 10^1122 times more than he loves us? See, I can do ID-math too.
The size of the sequence space is immaterial; what matters is how sparse are functional sequences amongst shorter peptides (say 15-30-mers) and, most importantly, how traversable the space is.
On the other hand, can you provide an example of someone designing a polypeptide de novo? The best example I can think of is taking the proteolytic cleavage site Arg-Arg, and enhancing it to Arg-Arg-Arg-Arg-Arg. I am not sure it qualifies as de novo, but it was a “1 in 8,000” long-shot (more ID-math(tm) ), and it worked!
Do I get an ID prize of some sort?
Just discovered a new planet. Planet Patrick!
Were you walking toward the moon or away from the moon? Were you walking toward the center of the earth or away from the center of the earth?
You haven’t demonstrated anything. You’ve merely imagined that you can walk 1000 miles because you can walk across a room.
Potential. Read for comprehension, dipshit.
The notion of a “proof of concept” is lost on some people.
colewd,
This is the bogus calculation of Hoyle, refuted a million times (or so). The alpha helix is a very simple, very common, readily adopted motif. There are countless squiddillions of different ways to get an alpha helix 141 acids long (then, I don’t think most are anywhere near that long).
There is software that can tell if an unknown sequence is an alpha helix or not. How? It does not have a database of all the possiblilities to look up. It does it on the pattern of acid properties. It’s that that determines folding.
In fact, you can get one turn of an alpha helix with a handful of acids (3.6 per turn). You can even get one out of a 2-acid library. Making its probability in the space so formed about 2^4. All you need to do to extend an a-helix is to end-join single turns. The probability of a two-turn helix from such a joining is not 2^8. And the probability certainly does not become 20^4 per turn simply by adding all 20 modern acids to the library.
“Why one hundred? If I were wrong, one would have been enough.”
— Albert Einstein in response to Hundert Autoren gegen Einstein (A Hundred Authors Against Einstein)
keiths,
This is a review from the book that you recommended. Thanks.
Have you tried to do simulations around the mechanism described in the book? The author is acknowledging the sequential space problem which is a good start.
From the same Amazon review:
Nice quotemine, dipshit.
Allan Miller,
I agree. Was simply describing the trial and error potential combinations. Where are we today in designing a new protein sequence that has enzyme function and understanding how sequence relates to final shape and function?
petrushka,
I was not trying to quote mine. I am asking about the authors thesis. Is this really a quote mine or his thesis? If it is a quote mine show me why I have taken a review out of context.
I already did. You inverted the reviewer’s intention by omitting the follow-up. That makes you a lying asshole, although I am sure you sincerely believe you are being truthful. Your sincerity is the scary part.
Are you too fucking stupid to understand the evolution is not a tornado in a junkyard?
Y’know, I was feeling I might have been a little harsh on this kid.
Emphasis on was.
Book reviews are interesting, but Amazon reviews are notoriously personal and variable in quality.
Anyone who wants to promote or mock a book can find a useful review.
If you would like to not appear ignorant, get the book and learn something. Then come back and discuss it.
colewd,
And not trying to make evolution look inadequate? I don’t see the relevance of the total permutations of a mechanism that no-one proposes to come up with a sequence no-one thinks is the sole possible functional sequence.
I can’t really give a sensible answer to that question. We’re ‘here’. We know ‘a lot’ about how sequence relates to form and function. Though folding is computationally very heavy. Which is why random libraries and selection tend to be used. Real things are better than models.
petrushka,
Here is the entire review. I am failing to see how what I pulled out is a quote mine.
colewd,
The first paragraph, without the rest, looks exactly like a quote mine. “Noted evolutionist X says how impossible evolution is”. Full stop. With the volume muted, noted evolutionist X goes on to say why evolution is not, in fact, impossible.
The scary part is that colewd doesn’t recognize the problem.
DNA_Jock,
Yes I have looked a Titan and understand that it is made up of alternative spliced exons and tandem repeats. Can you describe the source to the alternative splicing codes? Do you understand the sequential space problem? Do you know how the sequential space problem relates to alternative splicing? Szostak experiment shows binding to ligands. What is the most complex ligand it had blinded to? I did not realize that he had reached 100 poly peptide chains. How was the experiment set up?
Allan Miller,
Thanks for the explanation. I did not think the first paragraph did either, it was just ruling out random chance as the cause.
petrushka,
But why would you waste everyone’s time with a concept that isn’t now and never has been any part of evolution?
petrushka,
I was simply trying to be responsive to Keith’s point he was making and understand if this is really a new paradigm to get us closer to understanding cause. You thought I was trying to quote mine and I understand if you thought that was my intent it would upset you. It was not my intent. Just trying to understand more about the reference Keith’s gave me. So yes, you acted like a complete dick but I understood that you thought I was trying to mis lead so I cut you some slack.
I’m going to make one last non-snide and non-insulting attempt at communication.
Michael Behe (not Michael Denton) is an actual professor of biochemistry at a real (not fundamentalist) university. He is neither ignorant nor stupid. He is respected by Larry Moran, that atheistic evilutionist who says so many outrageous things and who fights openly with folks at Uncommon Descent.
Behe is at the very top of the heap in the ID movement. No one in the ID movement fights with Behe. He has the highest credibility in the ID movement.
Except that he adepts common descent. Reluctantly. He says he has no good argument against it.
He also argues that certain events in the history of life seem to have occurred against the odds. He is very specific and very limited in the list of these events.
He accepts that proteins can evolve and that their coding sequence can change over time. He does not argue against the thesis that neutral mutations change change genomes over generations.
So perhaps it would be a good idea for IDists to at least start at the level of Behe and not wast everyone’s time with tornado in a junkyard nonsense.
It would be nice if Denton would at least acknowledge that the most credentialed and competent IDist does not make this stupid argument.
Keiths recommended a book, and rather than read the book, or read and try to understand Wagner from some of his free, online essays, you pulled a quote from an Amazon review, an excerpt that misrepresented the intention of the review author, and you failed to provide a link.
Not the behavior of someone who desires respect.
Patrick,
I’ve moderated r/creation for two years. But having never visited there yourself you somehow know much more about it than I do? The majority of text I type in r/creation comments is debating our ID critics there. The next largest category is debating against ideas from other creation/ID people I disagree with. If you think it’s an echo chamber and do not trust me I would again invite you to contact our resident skeptics I linked above.
We used to be a public sub and ID critics outnumbered ID proponents about 10 to 1. We have around 1000 subscribers and reddit’s r/atheism has 2 million subscribers and our own posts would sometimes be crossposted there. It’s simply impossible to have a good discussion when so severely outnumbered–especially when the “lol skyfairy” crowd leads the parade.
Besides, I do regularly debate outside r/creation (and outside reddit) and so do many of our other members. Sal regularly invites our members to discuss here, and it was through one of his posts in r/creation that I found this thread.
Richardthughes, yes I’m the same JoeCoder from UD. Thanks for the welcome : )
Well good for you. Do you also understand that it shows all the hallmarks of having arisen via duplication? That was, after all, my question to you…
Somewhat incoherent question, as a response I will venture “random mutation and natural selection”…
Yes.
Yes. Alternative splicing allows proteins to tentatively explore distant sectors of sequence space, and move there only if they like the neighborhood. That’s quite the GSW to the foot you’ve got there, mate.
That’s right! And not, generally, enzyme activity. Glad I was able to teach you something. I guess. You’re welcome.
VEGFR-2 <ggg>
I’m going to let you figure that out for yourself, Dionisio.
DNA_Jock,
You did not understand the question: What is the source of the splicing codes not the cause? Why would you say random mutation and natural selection when you can’t identify the source?
Thank you. Yes I did learn something:-)
Can you point me to a citation? Dionisio?
petrushka,
I am not pro ID as far as a solution to identifying an evolutionary mechanism. I have read 2 of Behe’s books and think that he has interesting points but think irreducible complexity is a buzz word. I have read Hoyle’s tornado in a junk yard and understand its limitations. This does not take away from the fact the genome is a sequence and makes current proposed mechanisms problematic. Interestingly I think you believe this also from what I have seen from your responses. I appreciate DNA Jocks attempt to bridge the lab work and real world proteins. I was surprised that 100 amino acid proteins have been produced. I hope to understand the methods used. I agree that pulling that quote was a mistake. I am not an experienced blogger in this area and feel like a fish out of water because I am not attached to either side of the argument. I have thought you were somewhat in the middle also.
I don’t consider myself “in the middle,” whatever that means.
I don’t like ignoring the unsolved problems in science. Unfortunately for creationists and IDists, the unsolved problems don’t include many of their hobby horses:
Universal common descent
Human descent from apes
Evolution of proteins
Evolution of regulation
Isolated Islands of function
Stochastic mutation
Obviously biologists don’t know everything. they never will. But the Denton arguments are, at this date, flat earth arguments. He’s well past his sell by date.
But I will toss a bone to structuralism. The genes that control the expression of form evolved long before there were any multi-celled organisms capable of having form. It is possible that the list of possible body plans is constrained by these ancient genes. I don’t know that, but it seems possible.
If so, it does not validate Denton. It just means that rewinding Gould’s tape to the Cambrian might not make much difference. The constraints might be much older.
As for what causes patterns and forms, I’m reminded of Bill Cosby’s old question, why is there air?
I wonder if your toss missed its target. I don’t fully understand the structuralism argument, but my hazy understanding is that it claims structures are constrained by environments. There are only a few general possibilities for successfully navigating in the water or on land (or being immobile in either one), and these have been explored.
In other words, structuralists say the die was cast by the environment and not by what just happened to have developed in the earliest genes. Personally, I admit I had taken it for granted that the pretty much chance incidence of the earliest genes had bent the twig of life right at the inception. I understand physical constraints, but I think the variety of possible early genes is pretty much endless, and like Gould, I think if you rewind the tape early enough, you might not even get life as we know it.