No, not believe in science.
[quote=“Cornelius_Hunter, post:22, topic:9418”]
Another problem with this, following up on my comment above, is that there aren’t enough mutations to do the job.[/quote]
Sure there are! You’re just ignoring the vast majority of them.
[quote]The beneficial mutations in protein-coding genes, to evolve the human from a small, primitive ape, literally number only in the hundreds. It would be astonishing if the human could be evolved from so few mutations.
[/quote]It would be astonishing indeed. Is that why you’re ignoring recombination, translocation, and mutations in regulatory regions? These far outnumber the differences in protein-coding regions.
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The fact that the immune system routinely solves difficult binding problems is very germane to Bill’s point - he’s claiming that randomized processes cannot produce even one new protein-protein binding event (!). He’s claiming the problem is the vastness of sequence space. This is the exact same issue facing the production of antibodies by the immune system, and yet there is no problem at all in producing high affinity antibodies routinely. Merely claiming this observation is not relevant is not an argument.
Bill, if you’re interested in an example of evolution producing a new protein-protein binding event, I’ve written up an example here:
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Good point Ben and, no, I don’t ignore those–I separate them. One problem in evolutionary thought is that everything is viewed as fair game. So, for example, for epigenetics, evolutionists (those who are not still resisting), want to label it as just another facet of evolution.
Regarding the question of evolution of new species, not just by coding sequence mutations, but primarily by regulatory mutations, this raises more problems than it solves. I talk about this in my blog, and I’ve mentioned it here, in terms of the vast alternate splicing program in humans. Evolutionists figure that, given the few numbers of protein coding mutations, humans must have evolved by the alternate splicing of genes. That is an enormous problem just in terms of how that evolution could happen, but in addition to that, if it could somehow happen, it would be a striking confirmation of design, because it would mean that you have all these exons set up, a priori, which led to humans. Picture a factory that produces a whole bunch of parts, and in the end they just happen to all fit together to make a car. You can’t just willy-nilly throw anything you want into the evolution hopper. Epigenetics, regulatory evolution, etc., they don’t fit into evolution.
It is germane to Bill’s point only to the extent that Bill’s phrase (“a stochastic process”) can fairly be interpreted to include the mammalian immune system.
We could argue about semantics here, and what “a stochastic process” can mean. You could argue it entails the mammalian immune system (because there is a stochastic element to the whole thing). I could argue that it does not (because the the stochastic element would do nothing without an incredibly sophisticated search mechanism, wrapped around it).
But such an argument would, of course, miss the point entirely. The point is, there is no correspondence between the mammalian immune system and chance evolution. The former is set up to perform a great many “experiments” at a very high rate of speed, to measure the effectiveness of each outcome (the “fitness” if you will), to implement the solution, and so forth. The latter is completely different. To use the former as exemplary of, and justification of, the latter, is inappropriate. The former could be useful as a measure of the search space, difficulty, and so forth. But those results would then have to be cast into the completely different problem of chance evolution mutating, testing, selecting, etc. a modified protein.
So when cells replicate, all over the globe, for millions of years, and heritable variation is part of the mix, and not all variants replicate with the same success over that time period… somehow this is all completely different from what we see in the immune system? Why?
Also, I pointed out (to Bill) one case where a new protein binding site was evolved while scientists watched it happen. It involved random mutations and selection. Are you saying that new protein binding sites cannot evolve over time?
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According to that paper, except for in the cerebellum, humans have slightly less alternative splicing than chimpanzees.
I think you are looking at Figure 1A. Look at 1B.
Fig 1A and 1B tell the same story. According to their data,
- Overall, humans have about 2x more splicing than chimps, but (1B)…
- …that increase in splicing is entirely in the cerebellum (1A) and…
- …other organs (including the cortex part of the brain) actually have less splicing (1A).
So @glipsnort is entirely correct in his assessment.
So clearly, there is a lot of splicing in the cerebellum. But why? I bet most of it is neutral changes. In particular this quote from the paper is pretty remarkable…
Moreover, overall organ AS profiles more strongly reflect the identity of a species than they do organ type. This contrasts with organ-dependent differences in mRNA expression, which are largely conserved throughout vertebrate evolution.
So it has been known for a long time that most evolution at the mammalian level occurs by way of gene expression, small tweaks to proteins, and splicing changes. The origin of new proteins might happen occasionally, but this is relatively rare. This is one of the most remarkable and unexpected things in human genomes. We are made of the same “parts” as chimps, just “mixed” by splicing and expression in different ways.
Here is the kicker though, it is very easy to evolve new gene expression and splicing programs. Most gene expression and splicing changes are neutral with no effect, and there are several alternate ways to make the same change. So it is very easy to build up variation here that can be later selected. Because this accounts for the majority of changes we need to make a human from our common ancestors with apes, evolution here is actually very easy to imagine.
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Actually they do not tell the same story, but you will know that.
Again, no, not true. It is not true that this “been known for a long time.” In fact, it is not known to be true, period.
Again, this is not true. The search space is enormous and you have very little resources (in terms of Ne, timeline, and generation time). Its not gonna happen.
This is just so obvious that it is worth including the figures here. With the relevant caption…
Profiling of alternative splicing (AS) in vertebrates. (A) Relative proportions of exons undergoing AS in each sample, … (y-axis units relative to the sample with lowest AS frequency). … (B) Percentage of common AS events between human and other species., (C) Symmetrical heat map of Spearman correlations from PSI [splicing] profiles. For each sample, PSI values for the 1550 orthologous exons in the 11 analyzed species were estimated.
Reading this you can see figure 1A shows approximately equal amounts of alternative splicing for all samples except human cerebellum. Other than cerebellum, all other tissues measured have LOWER splicing than chimps.
Reading figure 1B, it is important to understand the axis first. Notice that humans have 100%? That is not because 100% of exons are alternatively spliced, but because 100% of human alternative spliced exons are alternatively spliced in human (by definition). The rest of the bars just show how many exons are spliced in both humans and each of the other species. About 50% are shared with chimps. The rest are not.
But we already know that there is a very large number of changes in the cerebellum (from Fig 1A). Looking at the high correlation (of about 50%) in figure 1C, we can be certain the bulk of the differences are in the cerebellum. Of course the data is available, so you can go test it yourself.
To be clear, this data is particularly problematic for any model that does not accept common descent.
First, there are a large number of “skipped” exons in humans and other species. We still see the exon, but is not used. Why is it still there? It is a lot like a pseudogene. Let me coin a term: a pseudoexon. This makes a ton of sense in common descent.
Second, why is that alternative splicing patterns are so species specific (Fig 1C)? In contrast, as a control, gene expression is much more tissue specific (Fig 1D)? This is exactly the same pattern (species specific rather than function specific) we see in neutral mutations (e.g. synonymous mutation) too. It is a clear signature of common ancestry.
Of course, we know that you (@Cornelius_Hunter) do not appreciate this evidence. That is fine. But what is your alternative explanation? Why do you see the patterns here that you do?
We keep asking for your model. We never get it…
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The search space is huge. And so is the solution space! It is huge also.
Especially with gene expression and splicing, there are many many ways to effect the same change. Uncountably many.
Also, gene expression is a very smooth landscape in sequence space, so it works great for evolutionary processes.
For these reasons, changing in gene expression by mutations is very very easy to do. We regularly see this happen even in human time scales. We see it in bacteria, cancer, in livestock and dog/cat/horse breeding programs. We see it in plants and more. This is so easy to do that it just happens all the time.
Of course, when we observe this, anti-evolutionists are quick to claim that this isn’t “really” evolution. Of course it is. In fact that is most of what we need to explain the evolution of new species.
Getting to the whole waiting time problem you raise. Our ancestors have explored billions and trillions of mutations since they diverged from chimpanzees 6 millions of years ago (try the rough calc. 6 million x 20,000 popsize x 100 mutations/gen / 15 years / gen). So we have very roughly trillion trials to tweak a few thousand gene expression and splicing signals, and there are many ways it can happen (there is not a unique solution), most of the differences we se are not even necessary (they are random drift), and sexual reproduction means they can happen in parallel (not one after the other). Remember we see this mechanism at play already on directly observable timescales.
There is more than enough time for evolution of gene expression. Remember, we see this already on an observable time scale. This is not particularly difficult.
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Hey Bill,
Did @DennisVenema’s response make sense to you?
I think this is a great example where we actually can test evolution directly. It turns out that it is very easy to evolve a new protein-protein binding site. We can even do this directly in the lab.
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[Did @DennisVenema’s response make sense to you?/]
Hi Joshua
I think Dennis brings up an interesting argument. I need to take a detailed look at it, hopefully tomorrow and will comment.
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[quote=“Cornelius_Hunter, post:28, topic:9418”]
Good point Ben and, no, I don’t ignore those–I separate them [recombination, translocation, and mutations in regulatory regions]. One problem in evolutionary thought is that everything is viewed as fair game.[/quote]
Your tendency to group people together and ascribe false positions to them does not contribute to dialogue.
So, for example, for epigenetics, evolutionists (those who are not still resisting), want to label it as just another facet of evolution.
How so?
But the statement to which you were responding didn’t mention alternative splicing.
There you go again. I suggest that you try to have a dialogue with people instead of making sweeping claims about what groups of people “figure.” Does that seem reasonable?
[quote]That is an enormous problem just in terms of how that evolution could happen, but in addition to that, if it could somehow happen, it would be a striking confirmation of design, because it would mean that you have all these exons set up, a priori, which led to humans.
[/quote]I don’t see how that’s the case.
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Hi Dennis
No one can say that a certain specific binding site cannot evolve over time especially if one is a few mutations away from another and you have the advantage of huge bacterial populations.
This does not model the search problems evolution is facing.
Your immune system idea is very interesting. Could the search algorithm Cornelius is referring to be a mechanism of evolution? I think the spliceosome and alternative splicing mechanisms that Joshua brought up are possible evolutionary mechanisms.
In the example I linked to, the new binding event is 4 mutations away from the starting point - far beyond Behe’s “edge of evolution” that the ID community likes to claim as a barrier for evolution.
You’re moving the goalposts here - you started out by saying randomized processes cannot generate new binding sites. I show you an example, and you fall back on saying it’s not relevant to your claim.
If modifying a protein to form a new binding site isn’t enough, we also have examples of enzymes being formed de novo, such as the nylonase example I’ve written up here. It arose from a frameshift mutation in a gene, giving a new open reading frame of 392 amino acids, that nonetheless was able to function as a weak nylonase. Subsequent duplication and mutation events to the duplicate produced a nylonase with much better functionality.
If sequence space is really too vast for evolution to work, why was this possible?
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This doesn’t work, and if it did, it wouldn’t be evolution. The latter first: For AS, or GE, or ATI/ATT, or epigenetics, etc., to create a human from a primitive ape would mean evolution had to have created 25000 genes, and the molecular mechanisms to create that change. If a factory created a bunch of parts which just happened to fit together to make a car, would you say it evolved? Of course not, this is silly. The fact that you insist this is evolution suggests you want evolution to be true. Indeed, even you had to admit how remarkable this is:
Indeed, from an evolutionary perspective this is astonishing. What luck? The level of serendipity is astronomical. Can you imagine the chance evolution just happened to create all that stuff, which incredibly turned out to make humans? I guess you could appeal to the anthropic principle, multiverse, and so forth. Evolution just keeps on surprising us.
Now the other problem is that all of this is unlikely anyway. The vast majority of our genes are alternatively spliced, and science indicates that, surprise, this is not merely useless diversity or junk DNA doing its thing. As this paper explains:
The history of evolutionary thought is full of claims of uselessness, only later to proven wrong. Alternative splicing looks to be quite useful and important. We have to assume that most of the human alternative splicing is important. No, that’s not to say you can’t change the splicing anywhere. But you probably can’t just have any old splicing patterns. The different alternative splicing of a gene can result in a very different gene product. So it is not good enough to just generate tons of AS, willy-nilly. It has to be the right AS, out of an enormous space of possibilities. Secondly, gene products typically work together. Sure there are singletons, but often proteins form quaternary structures, pathways etc. So most of these AS genes are going to function, at least part of the time, in a network, they need to come in groups. So a trillion mutations over 6 MY is not going to help. Drift over MYs is going to give some winners, but mostly a whole bunch of incoherent combinations. Selection isn’t going to work because you can’t get a group of newly created, coherent, ASs in one individual. You’re going to need a whole bunch of multiverses for this.
It sounds so easy doesn’t it? Evolution creates the genes, the introns / exons, the splicing mechanisms, the TFs, binding sites, and all the other regulatory machinery, and then it proceeds to experiment around, mutating these and building up a huge library of neutral functionality, and then at some later time, given a critical mass, or the right environmental shifts, that functionality now suddenly provides a coordinated orchestra of organization and emergent functionality. This is how evolutionists view the biological world, without concern for the serendipity.