Moving on to the next post from the other thread:
Oh God, tell me about it! I’m tired of trying to teach you basic molecular biology and evolution with every god-damned post in the vain hope we can even get to a stage where you understand the implications of your own arguments, but here we are.
No. Flat out incorrect. Ann Gauger and co-authors did exactly what I wrote. Exactly.
To clarify: They intentionally selected two functionally critical sites in the TrpA enzyme (that is responsible for synthesizing the essential amino acid tryptophan), then selected two mutations which in combination would render the enzyme nonfunctional, inserted the mutations into the gene encoding the enzyme, and then let the bacteria go on to evolve but with this nonfunctional enzyme being actively expressed. Only two specific reversals could then restore the enzymatic function of TrpA.
So even if, hypothetically, another compensatory mutational pathway to the restoration of function exists for these two specific disabling mutations, there’s no reason to think that hypothetical route is going to be as short/likely as the two direct reversals would be, so hence any such alternative pathway is unavoidably less likely than the double reversal itself.
So the gene trpA is now deleterious to the organisms, because it expresses a nonfunctional protein. Which costs the cells energy. Since the growth medium contains tryptophan already (otherwise the bacteria could not grow and divide, since the cells now lack the capacity to create their own tryptophan), the much more likely benficial mutational disabling of trpA expression (any mutation that reduces or abolishes trpA expression would now be beneficial as it reduces wasted energy) consistently occurred before any of the much more unlikely reversal mutation (many more mutations are possible that can reduce expression, than the only two specific reversals).
While another adaptive path was found immediately (abolish expression of trpA gene), it dit not involve the restoration of the function of the TrpA enzyme. The function did not re-evolve.
That’s not because two mutations is a limit. It’s because the other adaptive pathway was much more probable. So do you understand now how this paper cannot substantiate any claim that there’s a two-mutation limit to evolution?
Both great and fine? Well thanks.
Make sure going forward that you remember that the experiment detailed in that paper demonstrated that numerous adaptive pathways existed simultaneously, and that in multiple experimental re-runs different paths were taken. So this is a concrete empirical reality that organisms can find themselves in such a situation.
There were no such reasons stated in the post I was responding to.
Well you’re welcome to state what you think those reasons are instead of just declaring that you believe them to exist.
Then you have no explanation for the observation of ancestral convergence, and the data therefore de facto is evidence for common descent that (at least your version of) independent creation cannot account for.
Nothing stated by any EES proponent concerns the observation of ancestral convergence between phylogenetic trees derived from independent data sets.
I reiterate: Common descent predicts that as we go back in time on different phylogenetic trees, the data should become increasingly similar (we are getting nearer to a common ancestor). This prediction is overwhelmingly confirmed by comparative genetics.
I repeat. It is a direct prediction of common descent that we should see this pattern in the data. We do in fact see this pattern in the data. You have admitted you have no such prediction on independent creation. It is therefore evidence overwhelmingly favoring common descent and not favoring independent creation at all.
A brianfart of sorts? Fair enough, it happens.
I don’t particularly care when you put the divergences. I am pointing out what I see as a tension between two views you have expressed in your recent posts.
The two views are:
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On the one hand you think two mutations create a problem for the divergence of chimps and humans from a common ancestor, because that took much less than those >100 million years you think it takes for a function requiring two mutations.
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You must think innumerable other species do share common descent (say rats and mice for example, which diverged approximately 11-13 million years ago), which are at least as as genetically diverged as human-chimp, often even more so.
Do you start to see the problem?
I can’t make sense of the sentence “Bible readers have done just fine without knowing this” as a supposed response to what I am saying. Perhaps my point wasn’t clear, but I have now elaborated above.
Oh great, new function that requires two individually deleterious mutations then ala Behe & Snoke’s 2004 model, Right? Got any examples of those in humans or chimps?
Well for one we have zero evidence that any possible new function in the human lineage required two individually deleterious mutations. So even if we have a model that says such an event is unlikely to have happened in less than 100 million years, we have no reason to think it models anything that would have had to occur in the human lineage since the split from the human-chimp common ancestor.
Of course, there’s also the question of whether alternative pathways existed at the time, so even if such an individually unlikely path was taken it could just have been one out of numerous possible, greatly increasing the odds that at least one of them was taken.
To see what I mean consider this figure:
Grey arrows are mutational pathways that lead either to no new adaptations, or are much more improbable. Black arrows are the most likely pathways to new adaptations.
(A) Only one improbable pathways exists to one new function, all others lead to nothing (or are even more improbable). The scenario modeled by Behe & Snoke 2004.
(B) Several roughly equivalent pathways exist to the one new function. Even if any one specific pathway is unlikely, the fact numerous alternatives are possible increases the odds one of them will be found in the allotted time.
(C) Five possible new functions are available with roughly equivalent probability. As with B above, the fact that multiple are possible increases the odds that at least one of them will be found.
Of course you could combine them into a (D) option where five new possible functions exist, and all five each have multiple possible pathways to each of them.
It is no use only modeling scenario A and then pretending your work is done. To undermine evolution you also need to show options B, C, D etc. weren’t actual possibilities at the time the new function is inferred to have evolved. If you don’t do this work all you’re doing is assuming a restrictive scenario to get a conclusion you want. You have not demonstrated evolution is then unlikely, you have merely assumed it in a hypothetical model not based on empirical facts about the species in question.
Yes, in situations where we have reasons to think only scenario A is/was “in effect”, evolution is difficult and slow. It’s just we can’t just assume this is the case for some historical adaptation, since for every example we can find experimentally that conforms to scenario A, we can find others that conform to B, C, D etc. (I already showed you a paper that exhibits elements of both scenarios B and C as you agreed above).
Do you understand this?
Not exactly. Yes neutral mutations get fixed in the population as fast as they occur in a single individual, but that doesn’t mean all neutral mutations that occur in the population get fixed. The vast, vast majority are still lost.
It matters because it is out of this background rate of fixation of neutral mutations we get the degree of divergence between humans and chimps, for example. Some miniscule fraction of those have led to new adaptive factions in both species, but we have no evidence that they conformed to the scenario (A) above that Behe & Snoke models.
So the fact that the rate of fixation of neutral mutations is so high accounts for the degree of divergence of humans and chimps in those ~7 million years since our common ancestor.