What is Universal Common Descent?

That is a good point that for some people such common descent is uncomfortable. However, from a strictly scientific perspective, there are enormous problems. It is tempting to look at the high chimp-human genome similarity and think it is a strong confirmation of common descent. But there are all kinds of much more subtle differences. For example, humans have much more extensive, complicate alternate splicing of those genes.

Given the high similarity between the chimp and human genomes, and the relatively few beneficial mutations in protein-coding genes, evolutionists have considered the possibility of evolution by splicing. In other words, our enormous alternative splicing program may have been an important factor in our evolving from a small, primitive ape.

But there are many thousands of these gene splicing changes that would have to evolve. Given the relatively small effective population sizes, and long generation times, this is highly unlikely. And the problem quickly becomes even worse if groups of genes would need to implement their new splicing logic together. In fact, even if only the order of implementing splicing for a small number of genes is important, the problem quickly becomes even worse yet.

Furthermore, if this somehow could have occurred, it would make no sense on chance evolution given the incredible unlikelihood that exon boundaries would have just happened to set all this up. Like the DNA code, it would be another confirmation of design. There just is no free lunch.

Another problem with this, following up on my comment above, is that there aren’t enough mutations to do the job. 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.

@Cornelius_Hunter… again, I’m confused by your line of thinking. Are you saying that God could not have handled this? Everything you say seems focused on a dispute with someone who doesn’t believe in God.

But that’s really not the situation with the BioLogos audience… You understand that, yes?

George Brooks

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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:

http://biologos.org/blogs/dennis-venema-letters-to-the-duchess/the-evolutionary-origins-of-irreducible-complexity-part-4

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5 posts were split to a new topic: Josh and Cornelius get to know each other

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,

  1. Overall, humans have about 2x more splicing than chimps, but (1B)…
  2. …that increase in splicing is entirely in the cerebellum (1A) and…
  3. …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., © 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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@Swamidass

I copied an image of your attachment above, and ZOOMED IN …

… very valuable graphics !!!

[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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