Uncommon Descent Serving The Intelligent Design Community

Two Wrongs Don’t Make a Right

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

An article in Ecology letters, entitled: “Eco-evolutionary Dynamics in Response to Selection on Life-history,” deals with research conducted on “soil mites that were collected from the wild and then raised in 18 glass tubes.” The researchers
found significant genetically transmitted changes in laboratory populations of soil mites in just 15 generations, leading to a doubling of the age at which the mites reached adulthood and large changes in population size.

At Phys.Org, they write:

Although previous research has implied a link between short-term changes in animal species’ physical characteristics and evolution, the Leeds-led study is the first to prove a causal relationship between rapid genetic evolution and animal population dynamics in a controlled experimental setting.

Further, lead author Tom Cameron tells us:

“We saw significant evolutionary changes relatively quickly. The age of maturity of the mites in the tubes doubled over about 15 generations, because they were competing in a different way than they would in the wild. Removing the adults caused them to remain as juveniles even longer because the genetics were responding to the high chance that they were going to die as soon as they matured. When they did eventually mature, they were so enormous they could lay all of their eggs very quickly.”

Co-author Tim Benton states:

“This demonstrates that short-term ecological change and evolution are completely intertwined and cannot reasonably be considered separate.

There are two things to note:
(1) Darwin insisted on gradual change. This is not “gradual” change, but “rapid” change. You might remember those lizards on the Adriatic Islands that developed cecal valves in probably 20 generations or less.
(2) The vacuousness of the phrase “evolutionary change.” The term that should be used is “adaptive change,” for that is EXACTLY what is happening. The organisms doesn’t change in a way that has any evolutionary importance; it just simply changes.
(3) This “rapid” change indicates that “gene frequencies” cannot be changing, simply because the changes are occurring too rapidly. So, the likely instrument of these “rapid” changes is a change in gene expression, and hence, the turning on, and the turning off of gene promoters, which can easily happen via RNA–and, it can happen in a way that is inherited a la “Lamarkian” notions–not Darwinian.

None of what is being reported is consistent with either Darwinian, or neo-Darwinian, mechanisms. This is just a plain fact. You see, two “wrongs”—being wrong in the Darwinian and neo-Darwinian sense—does not make a “right.”

But “true believers” never let facts get in the way. However, there are so many of these inconvenient facts that day-by-day are collecting that it is but a matter of time before the whole Darwinian artifice comes tumbling down.

Comments
wd400: Yeah. Amazingly enough if you ignore for the source of new alleles you don’t get new alleles. If there is an insight in this I have failed to grasp it. Typical Darwinian response: you presume what you have yet to prove. Science is easy that way. You should have said this, which would have been more accurate: "Yeah. Amazingly enough if you turn off mutations, no new alleles show up." IOW, stasis is the rule. Now, you have to prove that "mutations" + NS can produce new alleles. wd400:
Alleles that are neutral today aren’t necessarily so in the future. Even slightly harmful mutations survive in small populations (search “nearly neutral theory”). It if very likely the accumulation of mildly deleterious mutations changes the fitness landscapes such that complexity can evolve (bacteria are too slick to allow the sort of mess our genomes accumulate). And you still haven’t accounted for newly-arising beneficial alleles. PaV: But doesn’t this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with?” wd400: 50 alleles? Which genes do you think have 50 alleles?
[Pardon the 'blockquote', but it was a pretty long quote.] " It is very likely the accumulation of mildly deleterious mutations changes the fitness landscapes such that complexity can evolve." It's "likely," but not known, I suppose. This, again, is typical Darwinian thought: what is "bad" for now, might be "good" later on. And then we can substitute almost anything we want for "bad" and "good", resulting in nothing more than equivocation. If some alleles were 'beneficial', and some were 'harmful', and the environment changes, then perhaps some of the 'harmful' ones become 'beneficial'; but, likewise, some of the 'beneficial' ones become 'harmful'. Touche. It's like a balanced polymorphism. Now, I ran the long quote up above for a reason: you ask now (why you didn't before is beyond me): "Which genes do you think have 50 alleles?" Well, maybe most of them. Just because population genetics doesn't take account of this genetical reality doesn't mean the reality doesn't exist. Why did Kimura propose his Neutral Theory? Do you remember? It's because he found so MANY polymorphisms!! Too many for neo-Darwinian theory to be able to account for due to the genetic load associated with maintaining each of these polymorphisms via positive selection. So he left Sewell Wright, and traditional population genetics behind, and proposed his new theory. And, of course, a "polymorphism" is just another way of saying "allele". So, in reality, each locus, when studied throughout a population, very likely has lots of polymorphisms/alleles, unless it's highly conserved. But, of course, if it's highly conserverd, then that means that NS is very busy weeding out additional polymorphisms/allleles. And this exactly proves the point I've been making: i.e., any given gene/locus has only so many possible permutations of a.a.s that NS will allow, and once those permutations have been explored, then the organism has no place to go: i.e., "stasis". And, of course, the fossil record shows, as Stephen J. Gould has written, that species "appear, continue on in the same way, and then disappear." Yes, that's right: "stasis." wd400: I didn’t give you terms in the hope you’d be impressed. I gave them in the hope you’d read about them and see the evidence for each model. You misunderstood me. What I said, I said 'tongue in cheek.' What I was saying is that you theorize this way and that, arrive at some conclusion, and give it a name. All of this "looks" like knowledge, when, in fact, it is the invention of names which can then be applied to certain situations in pop. gen. giving the appearance that all of these things are well understood, and conformable to reality. If you say somethng as stupid as “give me a 100 million years and you still won’t get a de novo gene” then I’m afraid you aren’t presenting an informed argument. I was just reading an article today on the Coelocanth---a living fossil. It's been around for over 300 million years (generations). It's still the same. Apparently no de novo gene there, eh. wd400: The outcome of a gene duplication is no a new allele, it’s a new locus. With one allele. Sorry you misunderstood this. What I was saying was not that an added allele now constitutes a de novo gene, but, rather, that very little "new" has happened---and so this is a very long stretch away from what we would expect for a true 'de novo' gene. Having said this, however, gene duplication---all by itself---simply reproduces an "allele" somewhere else on the genome. I.e., in, and of itself, there is no novelty. Let me just conclude with this: If---and this is a big 'if'---every living eukaryotic organism had the very same set of genes, then I would be convinced by this that "changing gene frequencies" can bring about evolution. OK. But this isn't the case. And recent evidence, as BA77 has cited, indicates that there are ample portions of 'de novo' genes that separate major lineages. Neo-Darwinism has not yet proposed a mechanism that can feasibly explain the appearance of said 'de novo' genes. When you come up with one, then, as Ross Perot said: "I'm all ears." In the meantime, epigenetics, inheritance via RNA, and other such things, are quickly undermining the entire relevance of population genetics, so complex is life. And I hope you continue to 'think outside the box.' It's good for science. But maybe more than just 'thinking outside the box', I have a very intuitive way of sizing things up---maybe it's the engineer in me---and, frankly, I don't see population genetics either now, or in the future, measuring up to the task of explaining cellular and biological complexity. After reading the 'bible' of population genetics, I just say: "This stuff can't be believed." Alas.PaV
April 18, 2013
April
04
Apr
18
18
2013
08:17 PM
8
08
17
PM
PST
which the HWE informs us ‘move around, but don’t change.’ Yeah. Amazingly enough if you ignore for the source of new alleles you don't get new alleles. If there is an insight in this I have failed to grasp it. I’m saying is that just like electrons in atoms can only enjoy certain energy states, so, too, you can only have “alleles” existing in certain configurations since either the changed a.a. is neutral, or more likely harmful, and so subject to elimination by NS Alleles that are neutral today aren't necessarily so in the future. Even slightly harmful mutations survive in small populations (search "nearly neutral theory"). It if very likely the accumulation of mildly deleterious mutations changes the fitness landscapes such that complexity can evolve (bacteria are too slick to allow the sort of mess our genomes accumulate). And you still haven't accounted for newly-arising beneficial alleles. But doesn’t this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with?” 50 alleles? Which genes do you think have 50 alleles? say that it’s always a good thing, when you’re in the ‘hand-waving’ business, to come up with new terms to dazzle others with . . . . Good job. I didn't give you terms in the hope you'd be impressed. I gave them in the hope you'd read about them and see the evidence for each model. I like thinking "outside the box" on pop. gen. The idea of close-minded academics is one of the most comically wrong cractitures going around. But you have to remember there is a great deal of evidence supporting the population genetics we have. If you say somethng as stupid as "give me a 100 million years and you still won't get a de novo gene" then I'm afraid you aren't presenting an informed argument. How in the world did you get the impression that I thought gene duplication was anything other than an added locus? Welll, you said "Wut doesn’t this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with? Where is the de novo gene in all of this?" The outcome of a gene duplication is no a new allele, it's a new locus. With one allele. I'm happy to think "outside the box" about population genetics, that's kind of my job. I just think maybe therewd400
April 17, 2013
April
04
Apr
17
17
2013
09:14 PM
9
09
14
PM
PST
PaV: Well, then, you begin with the HWE since mutation is “off”. This is “stasis.” Then you throw in ‘drift’, meaning that if part of the population gets seperated from the larger population, both the larger and smaller population form a new starting point for HWE. wd400: That’s not what drift means. Populations are not infinite, so allele frequencies (and, as we know from HWE genotype frequencies) change in each generation.The effect is more pronounced in small populations, since drift can be thought of as a population being sampled from the infinitely many potential populations made possible by the gene frequencies. You seem to have completely misunderstood what I was saying. I don't think it is because I didn't state it well enough. I think it is because you refuse to think outside of the box. You prefer rote answers. Yes, 'drift' means changing frequencies.** However, remember, that in the hypothetical I was dealing with, the environment was not changing, and an isolated, randomly mating population was assumed. Yet, it should be quite clear that I'm not interested in gene frequencies, which can, and do, change while HWE is present, but in the actual composition of alleles in the overall population---which the HWE informs us 'move around, but don't change.' The reason I mentioned 'smaller' and 'larger' populations is because when a population breaks up into 'smaller' and 'larger' sub-populations, then, and only then [assuming mutation is not at work, which was the assumption] do you have a 'change' in the number of alleles. And the number of alleles becomes smaller for both populations. This is the "loss" I talked about in an earlier post. **[If you look back at my post, I talked about 'phenotypic change'---that's the sort of thing that changed "frequencies" can bring about. (In fact you've quoted it below) But, again, it's insignificant 'microevolution', better described as 'adaptation.'] PaV: First, most mutations are harmful. Second, no “new” alleles have been formed. wd400: First, so? Second, yes they have. You say "so?". Alright. But this serves to highlight NS' true role: eliminate harmful genes. It's not in the business of developing "new" genes, but of getting rid of bad ones. "Yes, they have." How? How have "new" alleles formed? Did you follow the logic of my argument? What I'm saying is that just like electrons in atoms can only enjoy certain energy states, so, too, you can only have "alleles" existing in certain configurations since either the changed a.a. is neutral, or more likely harmful, and so subject to elimination by NS. PaV: That is, either the a.a. in the minor alleles are ‘neutral’, and NS doesn’t “see” them, or, if NS does “see” them, then if it is now “harmful”, NS will eventually eliminate it; and if it is ‘beneficial’, we’re almost exactly back to where we started from. Again, no “new” alleles. wd400: You missed the bit where you explain why we are “back where we started from” when newly arising alleles are beneficial. I also wrote later on---to clarify: "Now it may be argued that, under a changed “environment” some “new” allele, probably one that was ‘neutral’ at a particular a.a. location, but which now, with a changed a.a. at that former ‘neutral’ site, is non-neutral and beneficial, can, and does, occur. But doesn’t this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with?" Can't you see that an "allele" that represents a single a.a. change from another of the 50 "alleles" already present is, as I said, but as you wrongly quoted: " . . . almost exactly back to where we started from." Should we jump up and down and yell, "Alleleuia," because a single a.a. has changed on a string of 200 a.a.? Is this earth shattering change? Or is it almost an insignificant shift? I think common sense tells you it's the latter. PaV: So, while ‘drift’ can lead to phenotypic change and new-looking populations, nothing new has happened genetically. Thus, genetically, we’re dealing with a situation that is almost entirely analogous to “stasis.” wd400: No. I can’t see an argument in here to counter. You’ve just decided beneficial alleles take us back to square one, and decreed that changes in allele frequency aren’t evolution. You're completely unresponsive here. Changing allele frequency has a name for it: animal breeding!! But for you, it's "evolution." Tell me that this isn't exactly what happens when new breeds are come by: the gene frequencies have changed. And you call it "evolution" by decree. Wasn't Sewell Wright a "breeder"? Oh, yes, that's right; he was. He's the one who's given us adaptive landscapes and such, work that I admire; though I consider it now mostly wrong and outdated by the findings of modern molecular biology. And, again, you've simply (1) mis-characterized what I said, and (2) refused to think things through in a fresh way. What can I say? Tenure and prestige are powerful forces. PaV: And the conclusion there was, and still is: you’ve described “adaptation”; you haven’t described genetic innovation, as in de novo genes. wd400: No. Because I’m talking about what happened in 5 generations! I'll give you a 100 million generations, and you'll still not have a true de novo gene. Population genetics can't explain it---though they pretend to. I wonder: have you ever read R.A. Fisher's "The Genetical Theory of Natural Selection"? Are you aware of what his "fundamental theorem of natural selection" was based on? Just wondering. wd400: Life is chemisty. If you have a gene that does Job A very well it probably also does Job B poorly (search for enzyme “moon lighting”). Once you have a gene duplication one of the daughter genes is freed from the contstraint to perform JobA and can explore the surrounding sequence space. There is quite a lot of evidence for these sorts of models. Search “Subfunctionalization”, “neofunctionalization” and “innovation, amplification, divergence” for popular models. " . . . one of the daughter genes is freed from the constraint to perform Job A and can explore the surrounding sequence space." This is no more than "hand-waving." If you believe this stuff, that's your business. I know what it really is: navel-gazing at its finest. (If you re-visit what I wrote, you'll see that I have addressed this issue of "surrounding sequence space"** and have effectively argued that hardly any of it exists. OTOH, if we have a lot of imagination---as Darwin tells us we must---then I guess you can believe anything you want.) [N.B. I have to use this kind of edgy language because it's impossible to get you to think outside of the box otherwise; although I know full well that even edgy language isn't enough for that.] **[My essential argument up above is that this "sequence searching" will, in all likelihood, lead directly back to one of the 50 (now make it 51) alleles. IOW, the searching must, perforce, reach a limit. But, of course, Darwinists don't believe in 'limits.' After all, organisms are infinitely plastic, aren't they?] wd400: “Subfunctionalization”, “neofunctionalization” and “innovation, amplification, divergence” for popular models. I say that it's always a good thing, when you're in the 'hand-waving' business, to come up with new terms to dazzle others with . . . . Good job. And you say that they're "models"? Is this as in "climate change models"? PaV: Where is the de novo gene in all of this? wd400: Gene duplication means going from one locus to two. Is all this rant based on a misunderstanding of the term? How in the world did you get the impression that I thought gene duplication was anything other than an added locus? Isn't the language rather self-evident as to what it describes? Thus, your response appears to me to be a complete non sequiter. And why is what I write a "rant"? Because you're not ready to think it through, and not ready to change your mind about things? Is that it?PaV
April 17, 2013
April
04
Apr
17
17
2013
08:43 PM
8
08
43
PM
PST
Well, then, you begin with the HWE since mutation is “off”. This is “stasis.” Then you throw in ‘drift’, meaning that if part of the population gets seperated from the larger population, both the larger and smaller population form a new starting point for HWE. That's not what drift means. Populations are not infinite, so allele frequencies (and, as we know from HWE genotype frequencies) change in each generation.The effect is more pronounced in small populations, since drift can be thought of as a population being sampled from the infinitely many potential populations made possible by the gene frequencies. Now, we throw in mutation. Let’s assume there are 30,000 genes (loci). And let’s assume that there are two or three ‘major’ alleles (by this, I mean the most dominant alleles in terms of phenotypic expression) I wouldn't use the word 'dominant' like this while talking abut genetics. First, most mutations are harmful. Second, no “new” alleles have been formed. First, so? Second, yes they have That is, either the a.a. in the minor alleles are ‘neutral’, and NS doesn’t “see” them, or, if NS does “see” them, then if it is now “harmful”, NS will eventually eliminate it; and if it is ‘beneficial’, we’re almost exactly back to where we started from. Again, no “new” alleles. You missed the bit where you explain why we are "back where we started from" when newly arising alleles are beneficial. So, while ‘drift’ can lead to phenotypic change and new-looking populations, nothing new has happened genetically. Thus, genetically, we’re dealing with a situation that is almost entirely analogous to “stasis.” No. I can't see an argumentin here to counter. You've just decided beneficial alleles take us back to square one, and decreed that changes in allele frequency aren't evolution. And the conclusion there was, and still is: you’ve described “adaptation”; you haven’t described genetic innovation, as in de novo genes. No. Because I'm talking about what happened in 5 generations! When a Cadillac starts rusting, this is ‘phenotypic’ change, but it isn’t an instance of a way forward, but a way back wards. If a gene is left loose to mutate itself any old way, then here’s a question: what is different between taking any stretch of DNA, and then allowing it to mutate itself crazy over time, and having a “duplicated gene” mutate itself crazy over time? I see no real difference. Life is chemisty. If you have a gene that does Job A very well it probably also does Job B poorly (search for enzyme "moon lighting"). Once you have a gene duplication one of the daughter genes is freed from the contstraint to perform JobA and can explore the surrounding sequence space. There is quite a lot of evidence for these sorts of models. Search "Subfunctionalization", "neofunctionalization" and "innovation, amplification, divergence" for popular models. Where is the de novo gene in all of this? Gene duplication means going from one locus to two. Is all this rant based on a misunderstanding of the term?wd400
April 17, 2013
April
04
Apr
17
17
2013
03:46 PM
3
03
46
PM
PST
wd400: This is bizarre. HWE tells us how allele frequencies {A1, A2…} fall into genotype frequencies {A1A1, A2A1, A2A2 …} in the absence of any evolutionary force (including drift and mutation!). I don't think there's anything bizarre about it. The difference between you and me is that you very likely work at some college or institution, and, therefore, have no motivation or urge to think "outside of the box." OTOH, I have this luxury. And the curiosity. The bottom-line is that I have yet to discover any plausible mechanism for genetic innovation. Mircorevolution---which I consider a misnomer; the word that should be used is simply "adaptation"---is accepted by the vast majority of those holding to the ID view. So, for basically ALL of us here at UD, to talk about "microevolution" is of extremely limited interest. What interests us here is so-called "macroevolution." What I've been demonstrating (not just trying to) is that NS is a conservative force, HWE is a conservative principle of genetics, and that the mutation rate in most populations is not large enough to conceivably account for de novo genes. BA77 has a link to a very recent article demonstrating that there are genetic 'gaps' between major lineages. Neo-Darwinism has no answer for this, in my estimation. You can try to convince me otherwise, but, so far, you haven't said anything that I'm not familiar with or that remotely comes close to my changing my view. Let's look at the first part of your reply: Yes, HWE says exactly what you say that it it does, presuming random mating. It is a statement of stasis, is it not? I don't see how you can deny this. You, of course, will very quickly add: but there's always mutation and drift. Well, let's take a look first at 'drift.' We're considering now only 'drift.' Mutation is now out of the picture---at least for the time being. Well, then, you begin with the HWE since mutation is "off". This is "stasis." Then you throw in 'drift', meaning that if part of the population gets seperated from the larger population, both the larger and smaller population form a new starting point for HWE. But, again, in the absence of 'mutation', we have nothing more here than "stasis." I don't see how you can deny this either. Maybe you have some objection. Be happy to hear it. Now, finally, we couple 'drift' with 'mutation.' But, as has just been demonstrated, when 'drift' takes place, we're simply dealing again with the HWE, but now with new starting points. IOW, there are NO "new" alleles. Nothing "new" has happened genetically. Maybe something "new" has happened phenotypically; but not genetically (other than different gene frequencies based on the fact that there has been a re-shuffling of the original alleles: BUT, again, no "new" alleles---just different proportions [Again, 'microevolution'='adaptation' isn't of much interest here]). Now, we throw in mutation. Let's assume there are 30,000 genes (loci). And let's assume that there are two or three 'major' alleles (by this, I mean the most dominant alleles in terms of phenotypic expression), and a much larger number of 'minor' alleles. These 'alleles' will be characterized by different nucleotides and a.a.s along the length of DNA that codes for a particular gene (loci). If an average size protein has 200 a.a.s, let's say that 25%, or 50 of these a.a.s are NOT neutral, and can be considered an 'allele'. At the very least, if we look at the genome, we find 50 different locations along the length of the protein-coding portion of DNA where different a.a.s are found, and which might have some kind of functional activity (are non-neutral). If the population size is, let's say, 10,000, then, we have 30,000 loci, each having around 50 a.a.'s that have some slight, or major, phenotypic effect for each of these 10,000 organisms comprising the population. That means that there are: 10^4 x 3 x 10^4 x50 chances for a mutation to change an allele. This equals 1.5 x 10^10. Thus, with a mutation rate of 10^-8, each generation brings a potential change for 150 alleles. Now there are 3 x 10^4 x 50 alleles in the entire organism, or, 150 x 10^4. Obviously, in 10,000 generations, it is likely that each of these alleles has exprienced a mutation in some organism within the population. Is this, then, great news for neo-Darwinian novelty? No. And for two reasons. First, most mutations are harmful. Second, no "new" alleles have been formed. That is, either the a.a. in the minor alleles are 'neutral', and NS doesn't "see" them, or, if NS does "see" them, then if it is now "harmful", NS will eventually eliminate it; and if it is 'beneficial', we're almost exactly back to where we started from. Again, no "new" alleles. So, while 'drift' can lead to phenotypic change and new-looking populations, nothing new has happened genetically. Thus, genetically, we're dealing with a situation that is almost entirely analogous to "stasis." Please feel free to counter my argument. Again, in the little back-of-an-envelope example, the population went started with no individuals with beneficial alleles at all loci, and ended up with half of them being like this. Simply moving existing alleles around can profoundly change populations, and that’s evolution. (In fact, over short periods it’s like that most evolutionary change may come from standing variation, you ought to read a little about “soft sweeps” in the human genome). Of course selection removes variation, but mutation (and not , as you say, drift) introduces new alleles in every generation. None of this statement is inconsistent with what I wrote above. And the conclusion there was, and still is: you've described "adaptation"; you haven't described genetic innovation, as in de novo genes. The experiment you are talking about what carried out over a few generations, so it won’t have the answer to questions about how lineages that diverged tens of millions of years ago came to have different genes (loci). The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic. As BA77 has pointed out, this whole notion---the life-line of Darwinism---is now under a cloud and is being questioned. (So-called "pseudogenes", for example, formerly thought to be mere degraded duplicated genes, are now found to be involved in gene regulation.) Here again, though, one has to ask: what exactly is "new" when you have "gene duplication"? [As to "gene loss", a mild form of what happens through 'drift', obviously this cannot produce de novo genes. They might "look" different, but everything that is NOW there, was there before the change took place. Hence the "change" did not produce anything "new."] What we're told is that via gene duplication, a sort of 'spare' gene is now present in the genome, freed from any functional task, ready to mutate itself any which way. When a Cadillac starts rusting, this is 'phenotypic' change, but it isn't an instance of a way forward, but a way back wards. If a gene is left loose to mutate itself any old way, then here's a question: what is different between taking any stretch of DNA, and then allowing it to mutate itself crazy over time, and having a "duplicated gene" mutate itself crazy over time? I see no real difference. Now, you will likely object that we "know" that the 'duplicated gene' had function, and we don't know this about 'any' stretch of DNA. I concede this point. However, if this 'duplicated gene' had 'function' before, then, very likely, there are variants (alleles) of this gene throughout the population. Now, if something 'other than' one of these already present 'alleles' shows up---produced via mutation---then what should we conclude? I say that either: (1) the mutation is 'neutral', or (2) NS eliminates it if it is harmful, or (3) you simply end up with one of the already present alleles. Now it may be argued that, under a changed "environment" some "new" allele, probably one that was 'neutral' at a particular a.a. location, but which now, with a changed a.a. at that former 'neutral' site, is non-neutral and beneficial, can, and does, occur. But doesn't this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with? Where is the de novo gene in all of this? Please feel free to proffer a mechanism. I'd be happy to think about it. But I hope that in all of this, you can see that when I start thinking "outside of the box," I come up with no answers to my questions regarding "macroevolution" based on what population genetics wants to teach me.PaV
April 17, 2013
April
04
Apr
17
17
2013
11:10 AM
11
11
10
AM
PST
wd400:
The experiment you are talking about what carried out over a few generations, so it won’t have the answer to questions about how lineages that diverged tens of millions of years ago came to have different genes (loci). The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic.
Different genes? Evolutionism needs to explain new body plans and new body parts. And no one can link new genes to thoseJoe
April 14, 2013
April
04
Apr
14
14
2013
06:21 AM
6
06
21
AM
PST
semi related: Angolan Witch Spider, Giant Spider Found In Texas Is A Hoax… - March 24, 2013 Excerpt: Most spiders possess what are called “book lungs“, which are completely unrelated to what we normally call lungs, and developed independently. And from fossil evidence, we can determine that these structures have remained more or less unchanged throughout the past 400 million years because of how effective they are. There are downsides/limits to them though, with relation to lungs as we know them. As body size increases in relation to gas molecule size, they become less effective. This means that as animals with these structures get bigger they become less and less effective at “breathing”, which places limits on their maximum size. http://planetsave.com/2013/03/24/angolan-witch-spider-giant-spider-found-in-texas-is-a-hoax/bornagain77
April 13, 2013
April
04
Apr
13
13
2013
05:41 PM
5
05
41
PM
PST
wd400 you also claim that 'The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic.' Yet we find that,,
Evolution by Gene Duplication Falsified - December 2010 Excerpt: The various postduplication mechanisms entailing random mutations and recombinations considered were observed to tweak, tinker, copy, cut, divide, and shuffle existing genetic information around, but fell short of generating genuinely distinct and entirely novel functionality. Contrary to Darwin’s view of the plasticity of biological features, successive modification and selection in genes does indeed appear to have real and inherent limits: it can serve to alter the sequence, size, and function of a gene to an extent, but this almost always amounts to a variation on the same theme—,,, http://www.creationsafaris.com/crev201101.htm#20110103a This is the mother of all ad-hoc explanations: Phylogenetic patterns of emergence of new genes support a model of frequent de novo evolution - 21 February 2013 CONCLUSIONS: We suggest that the overall trends of gene emergence are more compatible with a de novo evolution model for orphan genes than a general duplication-divergence model. Hence de novo evolution of genes appears to have occurred continuously throughout evolutionary time and should therefore be considered as a general mechanism for the emergence of new gene functions. http://www.biomedcentral.com/1471-2164/14/117/abstract
Yup, Orphan genes (comprising 10 to 30% of every new genome sequenced, including humans) can now just ‘poof’ into existence. That whole evolutionary model of functional sequences being selected for in small increments is no good anymore. If you need a new gene you can just call on ‘de novo evolution’ to do your dirty work and once again evolution is protected from falsification:.
Orphan Genes (And the peer reviewed 'non-answer' from Darwinists) - video http://www.youtube.com/watch?v=1Zz6vio_LhY
Moreover wd400, there is experimental evidence against the whole concept of gene duplication being viable at the bacteria level,,
Experimental Evolution of Gene Duplicates in a Bacterial Plasmid Model Excerpt: In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence. http://www.springerlink.com/content/vp471464014664w8/
Now wd400, I know you believe in Darwinism with the faith that would make a suicide bomber jealous, but for those of us that find room to doubt that we evolved from pond scum could you please provide us some evidence that Darwinian processes can do what you insist they can do? Perhaps a falsification of this following null hypothesis if that is not too much to ask of you?
The Law of Physicodynamic Incompleteness - David L. Abel - August 2011 Summary: “The Law of Physicodynamic Incompleteness” states that inanimate physicodynamics is completely inadequate to generate, or even explain, the mathematical nature of physical interactions (the purely formal laws of physics and chemistry). The Law further states that physicodynamic factors cannot cause formal processes and procedures leading to sophisticated function. Chance and necessity alone cannot steer, program or optimize algorithmic/computational success to provide desired non-trivial utility. http://www.scitopics.com/The_Law_of_Physicodynamic_Incompleteness.html
You know wd400, with the continued failure of Darwinists to provide evidence for Darwinism to build functional complexity/information, I am really beginning to think that it is completely impossible for material processes to ever generate functional information! In fact (don't tell anyone), but I'm beginning to think that the first verse of John is actually true!
John 1:1 In the beginning was the Word, and the Word was with God, and the Word was God.
Music:
Creed - Bullet http://www.youtube.com/watch?v=KtCHFLMRX78
bornagain77
April 13, 2013
April
04
Apr
13
13
2013
05:13 PM
5
05
13
PM
PST
wd400, you claim:
the answer to questions about how lineages that diverged tens of millions of years ago came to have different genes (loci). The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic.
wd400, how come we can never seem to catch evolution in the act of evolving new genes and proteins? In antibiotic resistance, the most popularly known example of 'evolution', we find loss of information mutations all the time but never seem to find mutations on their way to building up functional complexity:
Is antibiotic resistance evidence for Darwinian evolution? http://www.youtube.com/watch?v=rYaU4moNEBU (Ancient) Cave bacteria resistant to antibiotics - April 2012 Excerpt: Antibiotic-resistant bacteria cut off from the outside world for more than four million years have been found in a deep cave. The discovery is surprising because drug resistance is widely believed to be the result of too much treatment.,,, “Our study shows that antibiotic resistance is hard-wired into bacteria. It could be billions of years old, but we have only been trying to understand it for the last 70 years,” said Dr Gerry Wright, from McMaster University in Canada, who has analysed the microbes. http://www.scotsman.com/news/health/cave-bacteria-resistant-to-antibiotics-1-2229183# List Of Degraded Molecular Abilities Of Antibiotic Resistant Bacteria: http://www.trueorigin.org/bacteria01.asp Unexpectedly small effects of mutations in bacteria bring new perspectives – November 2010 Excerpt: Most mutations in the genes of the Salmonella bacterium have a surprisingly small negative impact on bacterial fitness. And this is the case regardless whether they lead to changes in the bacterial proteins or not.,,, using extremely sensitive growth measurements, doctoral candidate Peter Lind showed that most mutations reduced the rate of growth of bacteria by only 0.500 percent. No mutations completely disabled the function of the proteins, and very few had no impact at all. Even more surprising was the fact that mutations that do not change the protein sequence had negative effects similar to those of mutations that led to substitution of amino acids. A possible explanation is that most mutations may have their negative effect by altering mRNA structure, not proteins, as is commonly assumed. http://www.physorg.com/news/2010-11-unexpectedly-small-effects-mutations-bacteria.html
Dr. Behe, as I'm sure you have been reminded again and again wd400, searched the experiments going back 4 decades, including Lenski's infamous LTEE and could find no examples of evolution generating new genes or proteins,,
“The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain - Michael Behe - December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/
Before that, as I'm sure you have been reminded again and again wd400, Dr. Behe examined the adaptations of malaria and HIV, which far outclasses the 'mutational firepower' of all higher life on earth for hundreds of millions of years and could find no instances of a gene or protein being generated,,
"The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable." - Michael Behe - The Edge of Evolution - page 146
wd400, you claim that 'lineages that diverged tens of millions of years ago came to have different genes (loci).' Yet if we look at ancient bacteria from 250 million years ago they are virtually the same at the molecular and morphology level as they are today.
The Paradox of the "Ancient" (250 Million Year Old) Bacterium Which Contains "Modern" Protein-Coding Genes: “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ; http://mbe.oxfordjournals.org/cgi/content/full/19/9/1637
The can confirm morphology even further back,,,
AMBER: THE LOOKING GLASS INTO THE PAST: Excerpt: These (fossilized bacteria) cells are actually very similar to present day cyanobacteria. This is not only true for an isolated case but many living genera of cyanobacteria can be linked to fossil cyanobacteria. The detail noted in the fossils of this group gives indication of extreme conservation of morphology, more extreme than in other organisms. http://bcb705.blogspot.com/2007/03/amber-looking-glass-into-past_23.html Static evolution: is pond scum the same now as billions of years ago? Excerpt: But what intrigues (paleo-biologist) J. William Schopf most is lack of change. Schopf was struck 30 years ago by the apparent similarities between some 1-billion-year-old fossils of blue-green bacteria and their modern microbial counterparts. "They surprisingly looked exactly like modern species," Schopf recalls. Now, after comparing data from throughout the world, Schopf and others have concluded that modern pond scum differs little from the ancient blue-greens. "This similarity in morphology is widespread among fossils of [varying] times," says Schopf. As evidence, he cites the 3,000 such fossils found; http://www.thefreelibrary.com/Static+evolution%3A+is+pond+scum+the+same+now+as+billions+of+years+ago%3F-a014909330
bornagain77
April 13, 2013
April
04
Apr
13
13
2013
05:13 PM
5
05
13
PM
PST
This is bizarre. HWE tells us how allele frequencies {A1, A2...} fall into genotype frequencies {A1A1, A2A1, A2A2 ...} in the absence of any evolutionary force (including drift and mutation!). Again, in the little back-of-an-envelope example, the population went started with no individuals with beneficial alleles at all loci, and ended up with half of them being like this. Simply moving existing alleles around can profoundly change populations, and that's evolution. (In fact, over short periods it's like that most evolutionary change may come from standing variation, you ought to read a little about "soft sweeps" in the human genome). Of course selection removes variation, but mutation (and not , as you say, drift) introduces new alleles in every generation. The experiment you are talking about what carried out over a few generations, so it won't have the answer to questions about how lineages that diverged tens of millions of years ago came to have different genes (loci). The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic.wd400
April 13, 2013
April
04
Apr
13
13
2013
03:32 PM
3
03
32
PM
PST
wd400: You have, indeed, reworded more or less what I wrote. As I said, if you start off with a population where it’s unlikely any individuals have at least one “beneficial” allele at each locus and end up with on in which most individuals do, then evolution has surely happened (even if you don’t want that to be called evolution, for reasons that remain your own). What I've tried to illustrate is that when this supposed process of NS is taking place, we're simply witnessing the 'loss' of 'alleles', with no more than a simple substitution of one 'allele' for another. with the former 'allele' going from 'beneficial' to either 'neutral' or 'slightly harmful', and the latter going from either 'neutral' or slightly harmful' to 'beneficial'. But nothing "new" has been introduced: we're just sliding things around. That was the reason for the calculation showing that there simply was not enough time for a "new" allele to have come int existence. So, if there is a possible 'loss' of alleles (that is, some very 'rare' alleles are completely lost to the population), and no "new" alleles forming, then, how can you begin to talk about "evolution"? It's just, at most, shifting things around (which is a mild form of 'stasis'). Which brings us to this: I’m not sure what your point about HWE is? Yes, if the assumptions of HWE held (and populations were infinte!) then no changes in gene frequency would be possible. They don’t. So? My point is that the HWE is a form of stasis, and, coupled to the fact that when the environment changes (and NS is assumed at play) "alleles" are either 'lost' or, at most 'shifted around', nothing new has happened. And, in the "new" environment, the HWE will take over. Repeat this process indefinitely, and, with eons of time, most of the "alleles" will have been lost, and genetic variance will be at a minimum, and, with the very next severe environmental change, extinction will take place simply because the "alleles" that used to get shifted to the 'common' frequency are no longer available, lost somewhere in the long stretches of time the species has been present. This fits the Fossil Record. But it means that "new" species have had to somehow been "front-loaded" because NS simply doesn't provide for "new" alleles. Genetic drift, given enough time, can restore some alleles that get lost along the way, but, overall, there is a downward trajectory as far as the number of alleles/genetic variance that is present. And, given the fact that de novo genes separate major lineages, somehow neo-Darwinism has to account for their origin. And I don't see any mechanisms being proposed that can overcome the incredible improbabilities of these coming about via random processes. Anyways, this is how I see things at present.PaV
April 13, 2013
April
04
Apr
13
13
2013
03:19 PM
3
03
19
PM
PST
wd400 you claim:
,,, if you start off with a population where it’s unlikely any individuals have at least one “beneficial” allele at each locus and end up with on in which most individuals do, then evolution has surely happened,,,
Do you mean that the neo-Darwinian version of atheistic evolution has surely happened? And that this provides scientific proof that microbes can turn into whales, elephants, and men? Surely even you know that this is far, far, cry from that level of scientific proof?!? If you are claiming this as proof for 'naturalistic/atheistic' evolution, then it is well to remind that even what are presupposed to be the purely random processes of the universe are now found to be dependent on a 'non-local', beyond space and time, cause in order to derive their most minute movement and even their 'being': i.e. Quantum Mechanics has now been extended to falsify local realism (reductive materialism) without even using quantum entanglement to do it:
‘Quantum Magic’ Without Any ‘Spooky Action at a Distance’ – June 2011 Excerpt: A team of researchers led by Anton Zeilinger at the University of Vienna and the Institute for Quantum Optics and Quantum Information of the Austrian Academy of Sciences used a system which does not allow for entanglement, and still found results which cannot be interpreted classically. http://www.sciencedaily.com/releases/2011/06/110624111942.htm Falsification of Local Realism without using Quantum Entanglement - (Where is the photon?) - Anton Zeilinger - video http://vimeo.com/34168474
i.e. Photons, on which everything in the universe is dependent on so as to derive their most minute movements, are found to require a beyond space and time, 'non-local', cause to explain their continued existence in space time. It is also very interesting to point out how these recent findings for quantum non-locality for photons, (and even for material particles), dovetails perfectly into some of the oldest philosophical arguments for the existence of God and offers empirical confirmation for those ancient philosophical arguments. The argument from motion is known as Aquinas' First way. (Of note, St Thomas Aquinas lived from 1225 to 7 March 1274.)
Aquinas' First Way - (The First Mover - Unmoved Mover) video http://www.youtube.com/watch?v=Qmpw0_w27As Aquinas' First Way 1) Change in nature is elevation of potency to act. 2) Potency cannot actualize itself, because it does not exist actually. 3) Potency must be actualized by another, which is itself in act. 4) Essentially ordered series of causes (elevations of potency to act) exist in nature. 5) An essentially ordered series of elevations from potency to act cannot be in infinite regress, because the series must be actualized by something that is itself in act without the need for elevation from potency. 6) The ground of an essentially ordered series of elevations from potency to act must be pure act with respect to the casual series. 7) This Pure Act-- Prime Mover-- is what we call God. http://egnorance.blogspot.com/2011/08/aquinas-first-way.html
or put more simply:
"The 'First Mover' is necessary for change occurring at each moment." Michael Egnor - Aquinas’ First Way http://www.evolutionnews.org/2009/09/jerry_coyne_and_aquinas_first.html
Not only is motion dependent on "Prime Act', i.e. a 'first mover', but quantum non locality also provides empirical confirmation for the philosophical argument from 'being', from 'existence' itself!
Aquinas' Third way - video http://www.youtube.com/watch?v=V030hvnX5a4
Thus wd400, no matter what motion occurs in the universe, one is forced to appeal to a 'non-local', beyond space and time, cause to explain that motion. Of course wd400, you could argue, as Charles Darwin did, that some actions/motions in the universe are so evil (earthquakes, hurricanes, diseases, etc..) that God would never allow those sorts of things to happen in this universe, but that would be a theological argument from theodicy, and would not be a 'scientific' argument for the validity of atheism/naturalism. To provide 'scientific' proof for atheism/naturalism, you would have to overturn either quantum non-locality for photons, or you would have to show that this 'non-local', non-material, beyond space and time, cause for motion and 'being' is consistent with atheism. Good luck with that endeavor wd400. Don't fret, obfuscation is easy for those bent on denying the reality of God. supplemental note; 'true randomness' does not exist in this universe in that a 'constant' is now found for what are perceived to be purely random processes:
The Austrian physicist Ludwig Boltzmann first linked entropy and probability in 1877. However, the equation as shown, involving a specific constant, was first written down by Max Planck, the father of quantum mechanics in 1900. In his 1918 Nobel Prize lecture, Planck said: "This constant is often referred to as Boltzmann's constant, although, to my knowledge, Boltzmann himself never introduced it – a peculiar state of affairs, which can be explained by the fact that Boltzmann, as appears from his occasional utterances, never gave thought to the possibility of carrying out an exact measurement of the constant. Nothing can better illustrate the positive and hectic pace of progress which the art of experimenters has made over the past twenty years, than the fact that since that time, not only one, but a great number of methods have been discovered for measuring the mass of a molecule with practically the same accuracy as that attained for a planet." (of note: Max Planck was/is a Christian Theist) http://www.daviddarling.info/encyclopedia/B/Boltzmann_equation.html
Verse and music:
Revelation 4:11 “You are worthy, our Lord and God, to receive glory and honor and power, for you created all things, and by your will they were created and have their being.” Acts 17:28 For in him we live and move and have our being.' As some of your own poets have said, 'We are his offspring.' Kari Jobe - Revelation Song - Passion 2013 http://www.youtube.com/watch?v=3dZMBrGGmeE
bornagain77
April 13, 2013
April
04
Apr
13
13
2013
03:33 AM
3
03
33
AM
PST
Tell me, wd400, the notion of “alleles”, does that come from Mendel or from Darwin? Bateson, actually. Tell me, wd400, your calculations of what happens in 5 generations, is that based on Darwin’s notion of gemmules, or is it based on Mendel’s Law of Segregation? It's based population genetics, specifically selection (Darwinian) and segregation (following Hardy and Weinberg's idea, which Mendel had no clue about, and most Mendelians failed to grasp). You have, indeed, reworded more or less what I wrote. As I said, if you start off with a population where it's unlikely any individuals have at least one "beneficial" allele at each locus and end up with on in which most individuals do, then evolution has surely happened (even if you don't want that to be called evolution, for reasons that remain your own). I'm not sure what your point about HWE is? Yes, if the assumptions of HWE held (and populations were infinte!) then no changes in gene frequency would be possible. They don't. So?wd400
April 12, 2013
April
04
Apr
12
12
2013
11:13 PM
11
11
13
PM
PST
wd400: Mendel didn’t have anything to say about that, nor did Messrs Hardy and Weinberg. Really? Do you want to stand by this comment? Tell me, wd400, the notion of "alleles", does that come from Mendel or from Darwin? Tell me, wd400, your calculations of what happens in 5 generations, is that based on Darwin's notion of gemmules, or is it based on Mendel's Law of Segregation? And isn't the Hardy-Weinberg Equilibrium based directly on this Law of Segregation while having nothing at all to do with NS, or anything else Darwinian? *** [see below] Would you like to answer these questions? Is it OK if I laugh a little bit in the meantime? wd400: The rest of it seems to be a rant about evolution not fitting your own misunderstandings of genetics and evolutionary biology. "A rant about evolution not fitting [my] own misunderstandings of genetics ..." Really? Please enlighten me (and any others who happen to take a look-see here at UD): I wrote this:
To this somewhat expected objection I submit the following analysis: Let’s suppose we begin with an organism which has, at “locus” L1, the following “alleles” in its population: A1,A2,A3….A_n. These have “frequencies” P1,P2,P3….P_n, respectively. “Selection” is presumed to be occuring at this locus. Your population genetics analysis tells us that, due to “selection” one (or possibly several) of these “alleles” will be favored. Thus, due to selection, with each passing generation, the population now contains the following “alleles”: A1,A2,A3…..A_n-1, A1,A2,A3…..A_n-2, and so forth, until, at last, A1,A2,A3……A_n-m. Correspondingly, for the last configuration of locus L1, the “new” “gene frequencies” are: P1,P2,P3,……P_n-m. All of these “frequencies” will have been found to be changed from those of the original population.
Now, please tell me where I have gone wrong in summarizing your understanding of what actually takes place as NS works on a population faced with a new, challenging environment. How have I misstated your analysis (other than what the actual dimunition of "alleles" looked like from one generation to another---a matter of little consequence here)? Let's remember that Kimura invented the Neutral Theory to deal with the unanticipated high level of protein polymorphisms found in the early 60's via gel electrophoresis, so I'm purposely not dealing with a 'two-allele per locus' model. (Yet, even with the 'two-allele' model, either (1) the 'rare' allele becomes very rare, but still present, or (2) it is eliminated from the population entirely, in which case, we have a "loss" of an allele, the very same point I was making. Either way, it's either stasis, or 'loss', and nothing new!) _____________________ . . . . . . ________ *** [In 1908 G.H. Hardy, a mathematician, found that in order for "a 3:1 phenotypic ratio to occur, the frequency of the dominant and recessive alleles each had to be 0.5, as they are a monohybrid cross between AA and aa parents", thus both alleles equal 1. The reason that he noticed this is due to Yule not observing that phenotypic frequencies are a direct function of the allele frequency. Also in 1908 Wilhelm Weinberg, a German physician, did ground breaking work using Mendel's principles. Shockingly enough, he was the first person to take Mendel's genetic principles and apply them to the human population. His work in addition to Hardy's basically related the frequency of genotypes to the frequency of alleles in populations. These two insights are known the Hardy-Weinberg Principle. Two conclusions come from this: The allele frequencies in a population will not change, generation after generation. If allele frequencies in a population are given by p and q the genetic frequencies will be given by p², 2pq, and q². -Basically this means p=A1(allele 1) and q=A2 (allele 2): they are both part of a larger statistical equation. Hardy and Weinberg used the p and q equations to find the genetic frequencies and the allelic frequency which is steady at all values between 0 and 1, as long as p+q=1. -(Jenkins, Simmions, & Snustad, 722) and (Freeman & Herron, 126-127). The Hardy-Weinberg principles will only hold true if all the assumptions of Mendel's law of segregation are not violated. In general they proved that, all things being equal (ceteris paribus), in the limits of those assumptions evolution does not happen. Yes, they proved that evolution does not happen. From the Univ of Dayton website on the Evolutionary Synthesis]PaV
April 12, 2013
April
04
Apr
12
12
2013
10:13 PM
10
10
13
PM
PST
Natural selection is not a magical ratchet and whatever is good enough gets to add to the population.Joe
April 12, 2013
April
04
Apr
12
12
2013
05:48 PM
5
05
48
PM
PST
All of what you write is based, not on Darwinism, but Mendelian genetics. Lol. Do you see the bit about selection? Mendel didn't have anything to say about that, nor did Messrs Hardy and Weinberg. The rest of if seems to be a rant about evolution not fitting your own misunderstandings of genetics and evolutionary biology.wd400
April 12, 2013
April
04
Apr
12
12
2013
03:17 PM
3
03
17
PM
PST
wd400: As an example, if you start with a single locus with two alleles with frequencies 0.1 and 0.9 respectively (such that the proportion of individuals with a at least one copy of the rare variant = 0.19). Now, imagine the environment changes that the rare allele is ~5 times more likely to survive than common one. Run the simulations an you’ll see in only 5 generations the frequency of the rare allele reaches ~0.85. 98% of the population have at least one copy of the newly beneficial allele. All of what you write is based, not on Darwinism, but Mendelian genetics. For example, you can use these very same numbers in a study about artificial selection. IOW, if Mendel's genetics had first been seized upon, rather than Darwinism, then they would apply to inbred populations. One then could extend this to the Darwinian idea of NS; but it would be an extension. Darwinism is not required for the numbers you propose. But now let me explicit about what I mean when I speak of "gene frequencies". First, I'm not talking about "allele" frequencies. The whole language of "loci" and "alleles" comes from Mendelian genetics and predates molecular biology. We now live in an age of WGA (whole genome analysis). It's a brave, new world. What I am talking about is genetic innovation: i.e., a "new" genetic solution to an environmental change. So, when I say that the "gene frequencies" don't change, I mean that no "new" genes have been developed. I am sure you would agree with me. You, however, might object, taking the position that since the "alleles" changed, this is tantamount to a change in "gene" frequencies. To this somewhat expected objection I submit the following analysis: Let's suppose we begin with an organism which has, at "locus" L1, the following "alleles" in its population: A1,A2,A3....A_n. These have "frequencies" P1,P2,P3....P_n, respectively. "Selection" is presumed to be occuring at this locus. Your population genetics analysis tells us that, due to "selection" one (or possibly several) of these "alleles" will be favored. Thus, due to selection, with each passing generation, the population now contains the following "alleles": A1,A2,A3.....A_n-1, A1,A2,A3.....A_n-2, and so forth, until, at last, A1,A2,A3......A_n-m. Correspondingly, for the last configuration of locus L1, the "new" "gene frequencies" are: P1,P2,P3,......P_n-m. All of these "frequencies" will have been found to be changed from those of the original population. And this is called:...............EVOLUTION! But why is this so? We know that if the "new" environmental pressures that brought about this change remain the same, then these frequencies will stay roughly the same. But, more than that, according to the Hardy-Weinberg Law, the actual numbers of alleles in the population (assuming the population size inbreeds and remains roughly the same size) will not fluctuate. This is STASIS, not EVOLUTION. And the thought experiment you're carrying out simply amounts to applying the Hardy-Weinberg Law with a "changed" number of alleles. This is like applying the laws of motion to a dynamical system that remains the same, but just simply starts out with different initial conditions. The "laws of motion" don't change; only the initial conditions. Applied to a population, this means that the Hardy-Weinberg Law---which results in "stasis"---is at work in a population until such time as environmental stress takes place. Under this stress, "ALLELES" are LOST!! Then, with a different array of "alleles" present, the Hardy-Weinberg Law is in effect once again. And "stasis" returns once again. What all of this demonstrates is that, with time, "alleles" are "lost", genetic variance decreases, and the ability of this particular "locus" to help the organism survive a new challenge is diminished. (With time, fresh mutations may restore, once again, the "alleles" that were "lost." But, given the size of the population, and other factors, this may take a considerable amount of time). So, based on what I've just described, what would we expect to see over long stretches of time: species appear, remain the same(the Hardy-Weinberg Law), and eventually die out (genetic entropy: i.e., they run out of "alleles" as they face "new" environment after "new" environment, and not enough time in-between to 'restore' the "alleles".) This is exactly what the Fossil Record portrays. Consult Stephen J. Gould on this. So, why on earth would you call this: "EVOLUTION"! I don't get it. Why not call it what it is: ADAPTATION. This "stasis" found in the Fossil Record suggests that the ability of an organism to 'mutate', with its concomitant 'harm' (most mutations are harmful---this has been demonstrated experimentally over and over) is 'balanced out' by NS, which simply eliminates what is harmful. And, that phenotypic and genotypic change can, and does, occur with 'changing environments', with the 'changing environment' simply 'changing' the 'definition' of what is 'harmful.' And the whole while, the organism remains roughly the same. And there you have it: NS is a force in nature that weeds out what is harmful in an organism. And, no more! Yet, what is left completely unexplained here, is this: How did the species 'appear' in the first place given that NS simply eliminates "new" (that is, 'harmful') "alleles." Where do the new "genes" come from? In strict analogy to classical dynamics, NS is a "conservative force." It's not an innovator or generator of anything. So what "force" is supplying these "new alleles"? Going back to what I wrote above, if, let us say, "allele" A_n-r, with r less than m, is removed from the population as a consequence of the "genetic load" experienced by the population under the new environmental stress, then it represents a "loss" of an "allele" with one, maybe two, particular amino acids located at very particular spots along the length of the "allele." If the "new" environment stays the same for a long stretch of time, then this "new" allele, A_n-r, is 'harmful' (that is, organisms with this "allele" died in the "new" environment, so, if they occur again, they will likely die once again since the environment is still the same. The population of the mites in this study was around 600. If A_n-r is to be restored---and using the easier case of just one a.a. substitution---then, given a mutation rate of, let's say, 10^-8, this means that to "restore" this "allele" the mite population would have to undergo 10^8/600 rounds of replication (generations). Or, 166,000 generations. And, if the environment hasn't changed, it will likely die, and the process has to begin again. If you counter with saying that in a larger population this needed 'mutation' would occur more rapidly, given that the environment has not changed back to its former mode, it's likely NS would remove it, or, at best, it would be subject to neutral drift, and a fixation expectation of 1/4N, which likely renders another large number. Noting these constraints, another question arises: how can you 'construct' an entirely "new allele" based on Mendelian genetics? And WGA tells us that, yes, indeed, there are de novo "genes" that differentiate major groups of species. So, how is this done? What is the mechanism? Two final remarks that put this last question into perspective: (1) Michael Behe uses the example of the malarial parasite to demonstrate (again using WGA) that it takes 10^20 replications of the malarial parasite population to come up with a 2 a.a. change in its genome in the face of eminent death due to chloroquine. Now, if, using the above example, the malarial parasite had these "alleles" already in place, then why did it take so long for this population to develop resistance to chloroquine: IOW, this demonstrates that we just can't assume that organisms have all their needed "alleles" already in place; and, that it takes a huge amount of replications [which is equivalent to time (yrs)] to 'find' these "new alleles". (2) Environmental pressures leads to a "loss" of information (in this case, "alleles"), rather than to any "gain." This is consistent with Behe's "Rule" for 'adaptation'.PaV
April 12, 2013
April
04
Apr
12
12
2013
12:35 PM
12
12
35
PM
PST
PaV #43: What, exactly, Nick, can possibly happen, from a statistical point of view, to gene frequencies with this number of genome replications? Any answers?
What exactly is the importance of this question, given the fact that changes in the genome are just part of a much bigger picture? What use are potentially beneficial DNA mutations without an appurtenant epigenome to guide them? Why zero in on DNA mutations and leave out numerous co-adaptations?Box
April 11, 2013
April
04
Apr
11
11
2013
06:19 PM
6
06
19
PM
PST
wd400, why is the fact that the vast majority of mutations are now shown to be 'non-random and targeted' not count against neo-Darwinism in the equations of population genetics?
Non-Random and Targeted Mutations (Epigentics to the level of DNA) - video http://www.youtube.com/watch?v=qTChu5vX1VI
wd400, why are 'fatal flaws' from population genetics ignored by Darwinists?
Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory - 2008 Abstract: Evolutionary genetic theory has a series of apparent “fatal flaws” which are well known to population geneticists, but which have not been effectively communicated to other scientists or the public. These fatal flaws have been recognized by leaders in the field for many decades—based upon logic and mathematical formulations. However population geneticists have generally been very reluctant to openly acknowledge these theoretical problems, and a cloud of confusion has come to surround each issue. Numerical simulation provides a definitive tool for empirically testing the reality of these fatal flaws and can resolve the confusion. The program Mendel’s Accountant (Mendel) was developed for this purpose, and it is the first biologically-realistic forward-time population genetics numerical simulation program. This new program is a powerful research and teaching tool. When any reasonable set of biological parameters are used, Mendel provides overwhelming empirical evidence that all of the “fatal flaws” inherent in evolutionary genetic theory are real. This leaves evolutionary genetic theory effectively falsified—with a degree of certainty which should satisfy any reasonable and open-minded person. http://www.icr.org/i/pdf/technical/Using-Numerical-Simulation-to-Test-the-Validity-of-Neo-Darwinian-Theory.pdf Mutations expressed early in embryonic development are the least likely to be tolerated by organisms – Paul Nelson – video http://www.metacafe.com/watch/5548184/ Understanding Ontogenetic Depth, Part II: Natural Selection Is a Harsh Mistress - Paul Nelson - April 7, 2011 Excerpt: The problem may be summarized as follows: -- There are striking differences in the early (embryonic) development in animals, even within classes and orders. -- Assuming that these animals are descended from a common ancestor, these divergences suggest that early development evolves relatively easily. -- Evolution by natural selection requires heritable variation. -- But heritable variations in early development, in major features such as cleavage patterns, are not observed.
wd400, If you can help me out with these questions and more like these, there is a job opening for you at Oxford!
Oxford University Admits Darwinism's Shaky Math Foundation - May 2011 Excerpt: However, mathematical population geneticists mainly deny that natural selection leads to optimization of any useful kind. This fifty-year old schism is intellectually damaging in itself, and has prevented improvements in our concept of what fitness is. - On a 2011 Job Description for a Mathematician, at Oxford, to 'fix' the persistent mathematical problems with neo-Darwinism within two years.
Music and verse:
Love the Lord w/ Lincoln Brewster http://www.youtube.com/watch?v=CV7qTD_X0Rk Luke 10:27 He answered, "'Love the Lord your God with all your heart and with all your soul and with all your strength and with all your mind'; and, 'Love your neighbor as yourself.'"
bornagain77
April 11, 2013
April
04
Apr
11
11
2013
04:54 PM
4
04
54
PM
PST
wd400, I appreciate you stopping by so as to straighten us out on population genetics. If you don't mind I have a few questions. How come the numbers don't work out here?
More from Ann Gauger on why humans didn’t happen the way Darwin said - July 2012 Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population. You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect. Facing Facts But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes. https://uncommondescent.com/intelligent-design/more-from-ann-gauger-on-why-humans-didnt-happen-the-way-darwin-said/
As well wd400, why is negative epistasis not seen as a falsification of neo-Darwinism using the equations of population genetics?
Mutations : when benefits level off - June 2011 - (Lenski's e-coli after 50,000 generations which is approx. equivalent to 1 million years of human evolution) Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually. http://www2.cnrs.fr/en/1867.htm?theme1=7 Epistasis between Beneficial Mutations - July 2011 Excerpt: We found that epistatic interactions between beneficial mutations were all antagonistic—the effects of the double mutations were less than the sums of the effects of their component single mutations. We found a number of cases of decompensatory interactions, an extreme form of antagonistic epistasis in which the second mutation is actually deleterious in the presence of the first. In the vast majority of cases, recombination uniting two beneficial mutations into the same genome would not be favored by selection, as the recombinant could not outcompete its constituent single mutations. https://uncommondescent.com/epigenetics/darwins-beneficial-mutations-do-not-benefit-each-other/ Response from Ralph Seelke to David Hillis Regarding Testimony on Bacterial Evolution Before Texas State Board of Education, January 21, 2009 Excerpt: He has done excellent work showing the capabilities of evolution when it can take one step at a time. I have used a different approach to show the difficulties that evolution encounters when it must take two steps at a time. So while similar, our work has important differences, and Dr. Bull’s research has not contradicted or refuted my own. http://www.discovery.org/a/9951
wd400, Why doesn't empirical evidence count against the equations of population genetics as empirical evidence counts against other mathematical models in other branches of science?
Waiting Longer for Two Mutations - Michael J. Behe Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that 'for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years' (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless "using their model" gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model. http://www.discovery.org/a/9461 Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) - October 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, "This research really upends the dominant paradigm about how species evolve," said ecology and evolutionary biology professor Anthony Long, the primary investigator. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_flies http://eebweb.arizona.edu/nachman/Suggested%20Papers/Lab%20papers%20fall%202010/Burke_et_al_2010.pdf "On the other hand, I disagree that Darwin's theory is as `solid as any explanation in science.; Disagree? I regard the claim as preposterous. Quantum electrodynamics is accurate to thirteen or so decimal places; so, too, general relativity. A leaf trembling in the wrong way would suffice to shatter either theory. What can Darwinian theory offer in comparison?" (Berlinski, D., "A Scientific Scandal?: David Berlinski & Critics," Commentary, July 8, 2003)
wd400, Why are most mutations hypothesized to be neutral even though the vast majority are now found to be slightly detrimental?
Unexpectedly small effects of mutations in bacteria bring new perspectives - November 2010 Excerpt:,,, using extremely sensitive growth measurements, doctoral candidate Peter Lind showed that most mutations reduced the rate of growth of bacteria by only 0.500 percent. No mutations completely disabled the function of the proteins, and very few had no impact at all. Even more surprising was the fact that mutations that do not change the protein sequence had negative effects similar to those of mutations that led to substitution of amino acids. A possible explanation is that most mutations may have their negative effect by altering mRNA structure, not proteins, as is commonly assumed. http://www.physorg.com/news/2010-11-unexpectedly-small-effects-mutations-bacteria.html
wd400, why are the population equations of the 'modern synthesis considered useless for the level of complexity we are dealing with?
The Fate of Darwinism: Evolution After the Modern Synthesis - David J. Depew and Bruce H. Weber - 2011 Excerpt: We trace the history of the Modern Evolutionary Synthesis, and of genetic Darwinism generally, with a view to showing why, even in its current versions, it can no longer serve as a general framework for evolutionary theory. The main reason is empirical. Genetical Darwinism cannot accommodate the role of development (and of genes in development) in many evolutionary processes.,,, http://www.springerlink.com/content/845x02v03g3t7002/
bornagain77
April 11, 2013
April
04
Apr
11
11
2013
04:49 PM
4
04
49
PM
PST
What, exactly, Nick, can possibly happen, from a statistical point of view, to gene frequencies with this number of genome replications? Any answers? Why don't you find out for yourself? As an example, if you start with a single locus with two alleles with frequencies 0.1 and 0.9 respectively (such that the propotion of individuals with a at least one copy of the rare variant = 0.19). Now, imagine the environment changes that the rare allele is ~5 times more likely to survive than common one. Run the simulations an you'll see in only 5 generations the frequency of the rare allele reaches ~0.85. 98% of the population have at least one copy of the newly benifical allele. Now step back and look at the genome as a whole. If 5 genes were subject to the same dynamics then before selection it's unlijely any individuals in the population would have at least one of the rare alleles at each locus (probability for each individual ~ 2e-4. After selection more than half would, and as a result your population would have changed considerably. Perhaps thinking through these things before you lean on the scorn button would be a good idea?wd400
April 11, 2013
April
04
Apr
11
11
2013
03:06 PM
3
03
06
PM
PST
Moderator: My last comments were completely off topic and I apologize. Regardless I believe AtS' questions, whether honest or not, are important.bb
April 11, 2013
April
04
Apr
11
11
2013
10:55 AM
10
10
55
AM
PST
ATS @57 "More important to whom, on what basis?" - To God, who created us to fellowship with Him. To us who can spend eternity in heaven or hell by choice. One would think that's pretty important. "If in your fallen world concept you deny man his goodness, then how can he be held responsible for anything?" - "No one is good except God alone." Mark 10:18 ESV The choice to follow or reject Christ with its consequences of redemption or damnation is before us. We will be held responsible for that choice. "Of almost no relevance to whom? Someone whose lived in a third world country for an extensive part of their life may find it to be highly relevant." - The key words in my comment were "compared to eternity". Suffering is important in that it elicits a response. The response, in the end, is more important than the suffering itself because it has eternal consequence. Suffering in this life is like a phlebotomy when compared to eternity. I agree with ba. I'm not convinced that you're a Christian. If not, would you like to become one? God's grace is there if you confess your sin and ask His forgiveness. Any suffering you may be going through may very well continue until the end of your life. But that's training and a constant reminder of our need for Him. It keeps us humble.bb
April 11, 2013
April
04
Apr
11
11
2013
10:35 AM
10
10
35
AM
PST
AtS: I have to say it is rather strange finding a professed Christian arguing against the "fallen world concept". But then again I didn't really learn that Christ was real until he he reached me in a moment of brokenness. Thus I have no illusions that man in his own goodness can merit eternal life. i.e. Grace!bornagain77
April 11, 2013
April
04
Apr
11
11
2013
09:02 AM
9
09
02
AM
PST
That life on this earth is short and fragile makes our choices more important. More important to whom, on what basis? That our life in eternity depends on those choices makes them of utmost importance. Do they really depend on those choices? If goodness is not that which promotes life, I'm not sure what is. If in your fallen world concept you deny man his goodness, then how can he be held responsible for anything? That life on this earth is so short compared to eternity makes our brief pain of almost no relevance. Of almost no relevance to whom? Someone whose lived in a third world country for an extensive part of their life may find it to be highly relevant. Only our response to that suffering matters. If the suffering does not matter, then why would the response matter?Aspire to Solomon
April 11, 2013
April
04
Apr
11
11
2013
08:37 AM
8
08
37
AM
PST
ATS @49:
And to suggest that that the life on earth that God made is, in essence, worthless, makes our choices in life of no consequence to neither God nor man, does it not? And if our choices don’t matter, and our bodies don’t matter, it’s hard to say that we matter at all, isn’t it?
No. That life on this earth is short and fragile makes our choices more important. That our life in eternity depends on those choices makes them of utmost importance. That life on this earth is so short compared to eternity makes our brief pain of almost no relevance. Only our response to that suffering matters.
For we know that the whole creation has been groaning together in the pains of childbirth until now.
Romans 8:22 ESVbb
April 11, 2013
April
04
Apr
11
11
2013
07:43 AM
7
07
43
AM
PST
I also think it's a bit of a stretch to say that Genetic Entropy = the fall. Are you saying that if the fall never happened, GE wouldn't happen? In that case, in such a place, how would things on earth be different, and why?Aspire to Solomon
April 11, 2013
April
04
Apr
11
11
2013
07:27 AM
7
07
27
AM
PST
Phinehas #44: Imagine the headlines if a similar goat were found in fossil form: “New transitional fossil found! Goat ancestral to Kangaroo!”
Phinehas, you raise a very important question. Given Slijper's goat - and many other cases of plasticity - what can we infer with certainty from paleontological evidence?Box
April 11, 2013
April
04
Apr
11
11
2013
07:14 AM
7
07
14
AM
PST
That's an interesting quote, but I'm not sure what it means.Aspire to Solomon
April 11, 2013
April
04
Apr
11
11
2013
07:01 AM
7
07
01
AM
PST
Your right, I don't have any empirical information to support my theological position; just intuition and the rules of logic, which in the absence of knowledge, is about as good as it gets.Aspire to Solomon
April 11, 2013
April
04
Apr
11
11
2013
07:00 AM
7
07
00
AM
PST
1 2 3

Leave a Reply