Progress after the Royal Society conference?

[Mercer (John Mercer)]

@lee_merrill

@Faizal_Ali

When the paper was published demonstrating that the reasons this trait evolved so rarely were not the reasons Behe claimed, he and the rest of the DI embarked on a campaign that brazenly and falsely declared that the paper actually vindicated Behe!

I wasn’t aware of this…

Of course you aren’t! You regurgitate Behe’s falsehoods without ever checking on their veracity. Even if someone points you to the relevant evidence, you won’t check before defending falsehoods.

[Mercer (John Mercer)]

@lee_merrill

Here is what Behe wrote:

It’s not true.

[Paul_King]

@lee_merrill

So how was Behe wrong? Details, please

It required multiple mutations, none of them simultaneous.

@lee_merrill

But the point was about Behe putting the limit at a “double-CCC”, not about the number of mutations for chloroquine resistance.

You can’t understand what Behe means by a “double-CCC” without understanding what Behe meant by a “CCC”. So yes it very much is about the number of mutations required for a “CCC” - and the simultaneity that Behe wrongly assumed.

[Rumraket (Mikkel R.)]

@lee_merrill

@Rumraket

@lee_merrill

Actually, all but one of Stadler’s referenced papers were apparently authored by evolutionists! Who show no evidence in their papers from what I saw, that they are sympathetic to intelligent design. So if so, these authors cannot be thinking people? And evolution was not said in any referenced paper as “giving up”. The experimenters eventually stopped their experiments, presumably after an appropriate and reasonable number of generations.

Obviously you understood that the conclusion you are claiming can be drawn from these papers is not actually believed by the world’s biologists. And yet you really do claim that this conclusion can be drawn from these papers.

It then follows that you are drawing conclusions from these that basically all the worlds evolutionary biologists disagree with. And yet you still think we should. That means you are positing an absurdity.

So how are the papers not saying they encountered a limit at about two mutations? Please show how this is not their conclusion.

By such a sentence not appearing anywhere in the result or conclusion.

Since it is a conclusion mistakenly drawn by creationists years after the paper’s publications, not by it’s authors.

@lee_merrill

And then show me where some biologists disagree with this limit.

Here on this very forum. In the various papers (by Michael Lynch and others) that have responded to Behe and others who have attempted to publish papers claiming such a limit. You should watch the video by evolutionary biologist @talkpopgen (Zach Hancock) I linked earlier.

In fact I can do better. Biochemist Michael Behe himself disagrees with it. In his first so-called waiting time paper (Behe & Snoke 2004) he writes(about the population sizes required to fix various numbers of individually deleterious mutations):

Such numbers seem prohibitive. However, we must be cautious in interpreting the calculations. On the one hand, as discussed previously, these values can actually be considered underestimates because they neglect the time it would take a duplicated gene initially to spread in a population. On the other hand, because the simulation looks for the production of a particular MR feature in a particular gene, the values will be overestimates of the time necessary to produce some MR feature in some duplicated gene. In other words, the simulation takes a prospective stance, asking for a certain feature to be produced, but we look at modern proteins retrospectively. Although we see a particular disulfide bond or binding site in a particular protein, there may have been several sites in the protein that could have evolved into disulfide bonds or binding sites, or other proteins may have fulfilled the same role. For example, Matthews’ group engineered several nonnative disulfide bonds into lysozyme that permit function (Matsumura et al. 1989). We see the modern product but not the historical possibilities.

This is Behe and Snoke admitting a colossal caveat with interpreting their results, and that the whole thing suffers from the hindsight thinking. Lynch 2005 demonstrated what happens for the waiting times if Behe and Snoke’s assumption of only a single set of mutations is violated (see figure 3).

@lee_merrill

If most biologists do disagree, this should be easy to point to.

It was.

[Rumraket (Mikkel R.)]

@lee_merrill

@Rumraket

@lee_merrill

Well, you trimmed my response, though I subsequently admitted that I misspoke. I meant that knock-out experiments are fine, not that selecting mutations to look for ahead of time is fine

Which is what you are doing when you search for two mutations which in combination renders a gene nonfunctional and where no other mutations can compensate, deliberately insert those two mutations, and then wait for those two and only those two to reverse.

But that is not my view, I would say the specific mutations would be anticipated to be the way function would be restored, but also any other mutations which restore function would be fine, too.

Who cares what you think is fine? What matters is what was done in the actual experiment, not whether you are personally okay with some alternative possibility that wasn’t explicitly tested. LOL.

@lee_merrill

@Rumraket

Not a particularly interesting or informative experiment with respect to evolution in general. The only sort of scenario for which such an experiment can be informative would be one where you know that some adaptation could only have evolved by such a pathway, and where no other alternatives existed at the time.

But I think allowing other mutations is fine too, you will get an idea how likely it is to restore function, regardless of how this happens.

Cool, but then there are lots of examples of knock-out experiments where beneficial genes are knocked out, the organisms then evolve to compensate for the loss. Typically these involve completely deleting the gene encoding some enzyme specialized for a particular substrate conversion, and what happens is the population adapts by mutations causing upregulation of another enzyme that has some promiscuous activity on that same reaction. Here’s a recent example, open access:

Adaptive laboratory evolution recruits the promiscuity of succinate...

In this paper we see how there are multiple routes by which the bacteria can compensate for the loss of two key enzymes (the strain is engineered both Δepd and ΔgapA). Generally, almost all involve ways of increasing the output of the sad gene. Either by gene duplications (more gene copies expressed = more enzymes), straightforward upregulation of expression, or mutations that increase the promiscuous activity, or some combination of two or all three. In fact the sheer number of ways there was for mutations to cause these compensatory changes was rather surprising, even including reductions in enzyme activity for enzymes active in other pathways (interesting how this biochemically led to increased sad expression btw.)

[Rumraket (Mikkel R.)]

@lee_merrill

@Rumraket

@lee_merrill

But no one who holds to separate creation says that the different proteins were created by chance! “Even on our conservative test, the probability that chance could produce the observed levels of ancestral convergence for just one of the eight datasets of 51 proteins is ≈1×10−19 and combined over 8 datasets is ≈1×10^-132.” But that’s the first I’ve heard of that view, I expect nobody subscribes to that.

Then why would separate creation predict ancestral convergence, the exact result expected on evolution?

But there are more than just two alternatives, randomness (which I don’t think anyone subscribes to), evolution, and special, intentional creation for which there is evidence that argues against evolution. Such as the various explosions of life forms (Cambrian, Avalon, etc.), such as the problems with the tree of life (e.g. orphan genes), such as the concerns some biologists have now about the origin of phenotypic complexity, and so on.

So what is the reason on special creation for forcing exactly the result (ancestral convergence) expected on common descent?

I mean, I assume you don’t think God is being intentionally deceptive by making the evidence look like common descent happened. So why does the evidence exhibit exactly the result expected on common descent?

Where is your model of the creation process that predicts ancestral convergence should result from it?

[Rumraket (Mikkel R.)]

@lee_merrill

@Rumraket

If two mutations are too much for 100 million years, how many species would need to be on the Ark if they are to have diverged that much from their common ancestors in less than 6000 years? Heck, even if you aren’t a YEC I think you need to think about how it possible so many species could show common descent with that degree of divergence if a mere two co-dependent mutations should represent a barrier to that. Could you be missing or misunderstanding something? Seriously consider that option.

You’ll not sure whether the Genesis flood was global, though, it might have been local, for example, a strong wind would not help in respiring a global flood.

That entire sentence does not parse meaningfully into english. Try again please.

Something about the flood possibly being local. Okay. What does that have to do with how many species share common descent, and how much they have diverged in the time since the supposed flood? By the way, how many animals were on this ark and when did the flood happen? This is a serious problem you have to deal with. If you think two populations can have diverged by no more than two mutations, how can you think even two individual human beings can be related?

@lee_merrill

But you need to address the problem of two mutations requiring about 100 million years for humans.

I already have, but seriously no that’s you who needs to do that. Handwaving in the direction of wind and local floods (wtf?) does not accomplish that. Dude wat?

[Rumraket (Mikkel R.)]

@lee_merrill

@Rumraket

How many of the “functions” in either species required (in order to evolve) two individually deleterious mutations that only in combination became beneficial, and where there were no other possible alternative mutation-combinations that could have provided the same or an equally adaptive function? We don’t know of even a single example.

I’m not sure what you mean, but I don’t require certain mutations were required, and that no other possibilities were possible, for a given function.

Then it isn’t clear why there is a problem at all. If you allow the possibility of many equivalent mutational sets, then there is no reason to think there’s a two-deleterious-mutation barrier to evolution.

It’s clear already you’ve never truly thought about this issue at all and you’re just spewing apologetic nonse you don’t understand.

I predict I will have to explain your own argument back to you next to even get you to realize why the creationist authors you rely on (such as Behe) have suggested something like a two-mutation limit to evolution.

@lee_merrill

@Rumraket

Have you heard of the neutral theory of molecular evolution and the rate of fixation of neutral mutations being equal to their rate of occurrence?

I have heard of the theory, but I don’t know what you mean by “rate of fixation of neutral mutations being equal to their rate of occurrence”.

Google it.

[Roy (34-year veteran)]

@lee_merrill

I was saying that Roy’s complaint does not describe Statler’s (or my) view.

My complaint was about you misrepresenting the contents of the video you linked to, not about anyone’s view.

Though I’m not surprised you are avoiding that fact.

[John_Harshman]

@lee_merrill

@Rumraket

Then why would separate creation predict ancestral convergence, the exact result expected on evolution?

But there are more than just two alternatives, randomness (which I don’t think anyone subscribes to), evolution, and special, intentional creation for which there is evidence that argues against evolution. Such as the various explosions of life forms (Cambrian, Avalon, etc.), such as the problems with the tree of life (e.g. orphan genes), such as the concerns some biologists have now about the origin of phenotypic complexity, and so on.

Ah, I see we’re back to my topic. And I see Lee has forgotten everything I’ve ever said about it. I understand how he got the name “Dory”.

@lee_merrill

@Rumraket

Have you heard of the neutral theory of molecular evolution and the rate of fixation of neutral mutations being equal to their rate of occurrence?

I have heard of the theory, but I don’t know what you mean by “rate of fixation of neutral mutations being equal to their rate of occurrence”.

Oh dear.

[Mercer (John Mercer)]

@lee_merrill

@Rumraket

Have you heard of the neutral theory of molecular evolution and the rate of fixation of neutral mutations being equal to their rate of occurrence?

I have heard of the theory, but I don’t know what you mean by “rate of fixation of neutral mutations being equal to their rate of occurrence”.

Have you considered the possibility of learning about it?