Comments on Bill’s math class

Conversation Side Conversation
,
163

No it doesn’t.

Lynch actually models the time to fixation under a range of possibilities, instead of restricting his case to just Behe’s.

As Lynch writes:

Second, Behe and Snoke assume that only two specific amino acid sites within a protein are capable of giving rise to a new selectable diresidue function. Given that the average protein in most organisms contains between ∼300 and 600 amino acids, this assumption is also unrealistic. Increasing the number of participating amino acid sites from n =2 to just 10 can magnify the probability of neofunctionalization by more than 10- fold

A range depending on assumptions
A range depending on assumptions875×797 76.4 KB

Notice how as the number of sites that can potentially participate in the specific multi-residue function increases, the arrival time to that specific result still decreases exponentially.

And he explains what the problem with Behe’s Texas sharpshooter fallacy is, as you saw above. That’s why he concludes:

In summary, the conclusions derived from the current study are based on a model that is quite restrictive with respect to the requirements for the establishment of new protein functions, and this very likely has led to order-of-magnitude underestimates of the rate of origin of new gene functions following duplication. Yet, the probabilities of neofunctionalization reported here are already much greater than those suggested by Behe and Snoke. Thus, it is clear that conventional population-genetic principles embedded within a Darwinian framework of descent with modification are fully adequate to explain the origin of complex protein functions.

And it still has nothing to do with Howe et al.

6 Likes
164

That model is a tree. That explains the pattern. You aren’t even talking about the pattern, though you seem incapable of realizing it. You’re talking about the number of events that make up the pattern, quite a different thing. The pattern is explained without any need to appeal to the causes of the events.

Nor have you given any reason to suppose that known processes are incapable of explaining the number of events.

Now, your problem seems to be with gains only, not losses. Is that correct? Because there’s good independent evidence for losses, i.e. the pseudogenes remaining after loss of the functional gene.

You have not shown that Behe’s model, much less Lynch’s model, is incompatible with the number of gains required by the diagram.

8 Likes
165

@colewd I wonder what is going through your mind. You ignore all of my posts, and even deny the factual basis of their contents in response to other posters. It’s really odd behavior.

You make claims that Lynch agrees with Behe, or is modeling the same things. But I’ve shown they don’t. With quotes, and the figures in their respective papers show that their different simulations do not obtain the same results. Even Behe himself gives entirely reasonable caveats about the results of his work in his own paper.

And then you mysteriously try to connect Behe’s one specific, highly restricted scenario, to all the gene gains in the venn diagram. But with no explanation for how you connect the two. You just sort of claim or assume Behe’s model–which is not the same as Lynch’s and gives radically different results and Behe himself admits have several caveats and pitfalls they did not explore in their simulations–is somehow the only valid way to model gene gain.

And yet, here you are repeating stuff we have all now read and seen for ourselves is either untrue, is inexplicable, or makes no sense.

This behavior is bizarre.

6 Likes
166

I had a dog who disliked baths. When we insisted anyhow, he would stand in the tub with one paw lifted out of the water, in mute defiance. And after we wetted and soaped that paw anyhow, he would lift it up, as though it did some sort of good.

I think that Bill thinks the object of argument is not to demonstrate a point, but to convince a person. As long as he can lift that paw, soapy though it may be, in defiance, he thinks he’s “winning.” If your object is to convince him, then he “wins” by being obstinately ignorant (and, with that, completely forgetful of all the past times he’s been shown to be grossly wrong).

But if his object is to convince a reasonable observer – and if yours is, too, well – the whole thing’s been over for years and there’s no room to doubt the outcome.

7 Likes
167

And recombination is required for accurate meiosis. Genetic defects in recombination cause macro genetic defects, particularly trisomies and monosomies.

My point is, @colewd, that your pretending that recombination isn’t a major contributor to genetic variation is incredibly ignorant and/or dishonest.

We have them. You don’t appear to be able to understand mathematical models.

Because you won’t, or can’t, do basic math.

You have put forth zero mathematical effort. Why is that, Bill?

Word salad. Evidence might show limitations. Models can’t. Besides, you can’t even describe the existing mechanisms.

4 Likes
168

We agreed that Lynch and Behe’s model were more favorable depending on the type of protein. This is a logical conclusion based on different preservation among proteins.

If these models were close to explaining the various Venn diagrams there may be a discussion. They are not close Rum and this quite obvious.

It is also quite obvious that multiple origin models need to be explored as we have been discussing this for five years now and it is obvious the gene duplication and divergence cannot explain the single origin models.

If your posts are straight forward then I will answer them. When you make cherry picked arguments it is not a good use of time for either of us.

169

They explain it perfectly, you’re just bad at math.

1 Like
170

It is not Lynch and Behe (they did not write a paper together, Lynch rebutted Behe and Behe agreed Lynch’s rebuttal is valid), it is Lynch or Behe. Their radically different models do not agree, and I do not agree their different models apply to any real scenario.

Even Lynch’s paper is still based on the Texas sharpshooter fallacy(in that Lynch too models the origin of a specific function in a specific set of duplicates). He just corrects a number of flawed assumptions in Behe’s model, to show that even using the Texas sharpshooter fallacy Behe’s numbers can still be radically improved with more realistic assumptions.

All of this I have quoted extensively. We can see the figure in my earlier post.

Interestingly Behe himself admits this in his paper. Lynch correctly points this same fact out.

No, how conserved a protein is, is not an indication of how it first evolved. And the inference of conservation requires common descent, which Behe agrees to. There is no such thing as a protein that is “conserved” between mice and humans, for example, if they have separate origins.

You can’t show this with any math. You don’t know how to do the math and you constantly distracted from any calls for you to do it. You can’t connect Behe’s scenario to any real protein, much less any from the ones counted as gained in the venn diagram from Howe et al.

Not a single one. You know of no actual example of a protein that had to evolve according to Behe’s scenario. It is a fantasy and no reality conforms to it.

If mere assertions such as these suffice in place of arguments and evidence, then mine is as good as yours. So here we go:
It is also quite obvious that multiple origin models do not need to be explored as we have been discussing this for five years now and it is obvious the gene duplication and divergence can explain the single origin model.

My posts are in fact straight forward. Plain, simple, easy to understand. And frequently come with links and figures, and I take care to explain principles and the logic behind inferences I or others make. I quote extensively from material we discuss, and nothing is cherry picked. I have actually been commended by other people here, who are creationists, for this fact.

You may ultimately disagree with the conclusions I come to, but not for any of the reasons you state. Those reasons are false and you constantly falling back on them reveals more about your character than anything else.

6 Likes
171

Your posts are not looking at the evidence realistically.

Ligands need a binding partner to do real biology. They needed mutations that bind to a receptor protein. Your Texas sharp shooter claim is not valid. A protein is useless with out other proteins to bind with and in these cellular pathways it is often several proteins. The ability to bind with a single receptor or dozens of different proteins and perform complex functions takes sequence specificity. The sequence preservation of proteins like beta catenin illustrates this.

You’re not looking at the problem and considering all the data. Especially the gene patterns and how a mechanism like gene duplication and variation could account for the pattern given its limitations and long waiting times to fixation.

Again, we have been discussing this for 5 years with no proposed model and no proposed change of the single tree outside the Creationist groups. Were stuck.

172

Behe disagrees:

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.

You have no math. Behe’s do not apply by his own admission.

2 Likes
173

Binding is extremely easy. Highly specific binding may not be, but low-level binding is common enough.

Why just another protein? What about binding to a different molecule? A bit of RNA or DNA? A lipid? This is part of your TSS.

For that matter, imagine a receptor kinase has been duplicated. A single mutation might remove the phosphorylation site, meaning expression of the duplicate would protect the receptor from phosphorylation by the original protein. Or a single mutation might prevent the duplicate from binding to the receptor, meaning the duplicate would compete with the original for ATP. Either of these would have a function, with a single mutation. It is flatly false to claim that multiple mutations are required for novel function.

We’re all still waiting for you to give the per generation rate of gene duplication. Which you necessarily must know to make any claim about it. Why are you unable and/or unwilling to provide this number?

3 Likes
174

Protein specificity is not binary.

Has this or has this not been discussed in previous threads?

We have just witnessed dozens, possibly hundreds, of protein variants that bind with ACE2 receptors, each and every one. Lots and lots. Like all of them, not just one specific sequence but all of them, totally stick to the same receptor.

3 Likes
175

This is trivial compared to the number of AA arrangements. Structural and functional properties of SARS-CoV-2 spike protein: potential antivirus drug development for COVID-19 | Acta Pharmacologica Sinica

SARS-CoV-2 is a single-stranded RNA-enveloped virus [5]. An RNA-based metagenomic next-generation sequencing approach has been applied to characterize its entire genome, which is 29,881 bp in length (GenBank no. MN908947), encoding 9860 amino acids [6]. Gene fragments express structural and nonstructural proteins

The binding (S) segment is also quite large.

The total length of SARS-CoV-2 S is 1273 aa and consists of a signal peptide (amino acids 1–13) located at the N-terminus, the S1 subunit (14–685 residues), and the S2 subunit (686–1273 residues); the last two regions are responsible for receptor binding and membrane fusion, respectively.

176

I would consider that retention of function with a 10 percent substitution to be pretty permissive of variation.

And covid is just a example. If there is a cell receptor, there generally is a virus for it. Different proteins stick the the same ligand, and the same protein sticks to different ligands expressed in different species.

2 Likes
177

I would agree some proteins can vary this amount or more. What you’re not counting is fixation time in this case. You’re looking at the variation in the population.

How would we determine what the consensus sequence is as we can with vertebrates.

Interesting claim? What percentage of proteins do you believe this is true for in humans?

178

You’ve provided no evidence that fixation rate is a problem. You’ve only presented Behe’s nonsense, which is not relevant to the current conversation.

2 Likes
179

Sure, but variants did fixate in a matter of months or even weeks.

Genomic Surveillance for SARS-CoV-2 Variants: Predominance of the Delta (B.1.617.2) and Omicron (B.1.1.529) Variants — United States, June 2021–January 2022 | MMWR
Genomic Surveillance for SARS-CoV-2 Variants: Predominance of the Delta (B.1.617.2) and Omicron (B.1.1.529) Variants — United States, June 2021–January 2022 | MMWR1185×720 96.9 KB

4 Likes
180

^^^This, Bill. Please stop making this objectively false assumption.

I would add that exquisite binding specificity and affinity routinely evolve, increasing by many orders of magnitude, by variation and replication in only two weeks in the immune response. The fact that different people, even identical twins, produce different antibodies shows us that binding is common in sequence space.

Many times; so many that it seems likely that Bill is simply lying by invoking this falsehood today.

Why don’t those count, Bill? They evolved by common descent from a single ancestor in less than three years!!!

2 Likes
181

There is none. The consensus sequences are often artifacts of limited sampling that tell you nothing about variation, though, do they?

2 Likes
182

And notice that Behe isn’t piping up about SARS-CoV-2. If ID had any validity, one would think that the ID community would be front and center to help save human lives, no?

1 Like