Bill's math class

[Dan_Eastwood]

OK, this isn’t Beat Up on Bill Day. Wrong is wrong, and I see no point in allowing this to continue unchecked. We can re-open the topic in a day or two if anyone has constructive comments to offer.

[CrisprCAS9]

Note to everyone else: For Dan’s sake, be kind and careful if you decide to post. Assume I’ve got this.

@colewd

Behe and Lynch already did the math.

Then… what was it, Bill. Show your work. Specifically, your work that shows the math they did and how it’s relevant to this conversation. Because… it’s not relevant to this conversation.

@colewd

This one is not hard if you are willing foo face reality and look at the models, the available empirical data and the assumptions objectively.

I have, which is why I know the models are sufficient. I’m trying to get you to realize YOUR math, wrong though it is, STILL says the same. But… that’s why you refuse to actually do the math.

@colewd

can find new function

The data you say needs to be explained shows no evidence of new functionality. So… irrelevant. Since it’s irrelevant, any further mention of it will be ignored and this comment quoted.

@colewd

The comparative models above are for 2 changes.

And… zero coordinated changes are required to explain the data you say needs explaining.

If you have other questions… ask them. But if the question contains a mathematical assumption you will be asked to show the math before you get an answer.

[Rumraket (Mikkel R.)]

@colewd

The number of changes (Lynch 2 max Behe 6 max) in mammal gene families changes can exceed several hundred. (issue for both Behe and Lynch models)

Bill did you know that a corollary of Axe’s 2004 work, if we assume contrary to evidence that his number is correct, is that there are actually 20¹⁵⁰ x 10^-77 ≅ 1.43 x 10¹¹⁸ different possible, still functional TEM1 beta-lactamases.

That’s what Axe’s number means if we assume it is correct. That’s how many functional TEM1 beta-lactamases there would be in the total sequence space for a 150 aa protein, even if only one in every 10⁷⁷ was functional. 1.43 x 10¹¹⁸ different proteins.

The idea that a protein present in two different species can’t diverge by a hundred residues is a magnitude of error that is difficult to fathom. You don’t have to assume they gained new functions. They just diverged in sequence.

[Tim]

@colewd

There is no point here IMO as the time to generate a new gene based on Lynch’s estimates will exceed available evolutionary time and will also exceed Behe’s estimate

Whilst cognizant of @CrisprCAS9’s request that we keep the cacophony to a minimum, I think there is a conceptual issue here that should be addressed.

May I suggest that the “point” is that there is disagreement over whether the “estimates” in question entail that “the time to generate a new gene … will exceed available evolutionary time”.

Where such disagreement exists, the only viable solution is to perform a mathematical calculation that transforms the estimates into an explicit time estimate.

Further, I would respectfully suggest, that the person who made the original claim that “the time … will exceed available evolutionary time”, ‘bears the burden’ of providing the math to demonstrate the validity of this claim, where such disagreement exists.

Simply restating the original claim does not negate the disagreement, and so does not negate the point of having a thread like this to resolve this disagreement, and similar ones.

[Rumraket (Mikkel R.)]

@colewd

gene duplication and random change are not a viable explanatory mechanism for the observed diversity of genes in mammals

Show your work.

[Mercer (John Mercer)]

Bill,

You might learn something from these talks. Hopefully, the title will entice you:

The Evolutionary Design of Proteins: How does Protein Design Happen? • iBiology

[Puck_Mendelssohn]

I note that Bill has scarpered. I think that we have, there, an admission that he has not one thing to say in his own defense.

[Tim]

I think you underestimate Bill most dreadfully. He will admit nothing of the sort. As I said in an earlier thread:

@Tim

All the creationist has to do is ignore the claim or quibble over red herrings. Then they will go on the next day as though their argument was never defeated.

This thread never even happened, let alone stymied Bill’s claims, and he will be back repeating his claims within a very short period of time.

[CrisprCAS9]

At which point, I hope you point him to this thread and refuse to comment further.

[Rumraket (Mikkel R.)]

@colewd are you there? Gonna start doing that math and show your work anytime soon?

[CrisprCAS9]

The appropriate place for this comment, and for you to defend having posted it…

@colewd

Back then, chromosomes 12 and 13 fused together to create what we now call human chromosome 2. The fused chromosome then slowly spread through the community. And then, for some reason, the group of humans with 46 chromosomes eventually supplanted the group with 48.

From your citation.

What assumptions would have to be made for this to be feasible using a population genetics model?

Without this the author is begging the question. As he is ignoring the possibility that humans and chimps are separate kinds and humans always had 46 chromosomes.

The challenge to making a feasible model is the deleterious nature of chromosome change and the relatively low frequency of this type of mutation.

In the case of Rino’s and horses they are separated by 18 chromosomes. Rino 82 and horse 64.

[CrisprCAS9]

@colewd

I am simply applying reasonable assumptions to two models that were developed close to 20 years ago.

You should name those assumptions here, in the appropriate thread.

[Faizal_Ali]

@colewd

The assumptions are dependent on the gene/proteins that are observed. If the protein is not preserved across species then Lynch’s model is the most useful. If they are preserved then Behe’s model is the most useful.

For beta lactamase in bacteria I would use Lynch’s model for beta catenin or WNT 11 in vertebrates I would use Behe’s model.

Please show the calculations you have made to support the above assertions. Thank you.

[colewd (Bill Cole)]

@Faizal_Ali

Please show the calculations you have made to support the above assertions. Thank you.

It’s inherent in the assumptions of the models. Behe assumes most gene mutations are deleterious where Lynch assumes most mutations in genes are neutral.

Preserved genes are evidence that most mutations are deleterious.

Genes that are not preserved is evidence that most mutations are neutral.

[Faizal_Ali]

Please show the requested calculations. Thanks again!

[CrisprCAS9]

@colewd

Genes that are not preserved is evidence that most mutations are neutral.

Now take a moment to think about that statement in the context of the diagram you always say can’t be explained…

No preservation of those genes means… what?

[Faizal_Ali]

@CrisprCAS9

Now take a moment to think about that statement in the context of the diagram you always say can’t be explained…

No preservation of those genes means… what?

It’s such a pity that @colewd cannot appreciate what a great “Gotcha!” that is. But some of us do, at least.

[Art (Arthur Hunt)]

@colewd

Genes that are not preserved is evidence that most mutations are neutral.

So, @colewd, are you saying that, because beta lactamase and WNT11 are different (“not preserved”), most mutations in these two genes are neutral?

[colewd (Bill Cole)]

@Art

So, @colewd, are you saying that, because beta lactamase and WNT11 are different (“not preserved”), most mutations in these two genes are neutral?

Preservation is a protein that changes very little over time. If you look at beta lactamase it is not preserved between different bacterial species. WNT 11 mouse and WNT 11 human is over 97% identical in matched sequences.