It’s not about arguments. It’s about the evidence that you and Behe are ignoring.
@Rumraket didn’t say that. Specific examples are plentiful. Perhaps you should look at them instead of pretending that they don’t exist?
Please show the detailed math you did to support this grandiose claim.
Either that or they are pretending that selection doesn’t exist and evolution is random, without ever mentioning neutral theory, which is decades old.
The fixation waiting times are too long for either Behe or Lynches assumptions to find a unique sequence. They are only about 2 mutations taking up to 1 million generations. The math problem is obvious.
From L Morans critique
Behe & Snoke claimed that with two mutations you need a population size of 10^12 in order to fix the new allele in one million generations. The Lynch simulation shows that the new allele can be fixed in one million generations with population size of only 10^6 provided there are 50 potential mutable sites ( n =50). That’s a difference of six orders of magnitude.
Even with n =2 (as in Behe & Snoke) a population of one million could lead to fixation in 10^8 generations in the Lynch simulation whereas it would take 100 times as long according to Behe & Snoke. Recall that most of these simulations apply to single-cell, haploid organisms such as bacteria. In those populations the generation times can be measured in days. There might be 100 generations per year so 10^8 generations could be only one million years—a short time in the history of life.
Bill, I’m willing to believe you may have something to say, but that was still word salad. You should understand that most of the genes in that diagram are within widespread gene families, explainable by duplication and divergence. Your last sentence appears to mean nothing at all.
Thats right and this explains a gene with a few different substations (if Lynch’s assumptions are right) getting fixed in a population.
It does not explain how a unique gene that has many new mutations is generated and fixed in a population. The mutation and fixation mechanisms are not powerful enough to explain this observation.
You need to do math to know that. Please show the detailed math you did to support this grandiose claim.
Those are numbers, not math. Where is your math, Bill?
If it’s obvious, it should be easy to lay it all out. I don’t think you will.
Quoting people isn’t doing math.
You haven’t shown the slightest indication that you understand the genetics, the biochemistry, or the math. Please stop pretending and making claims about things you obviously don’t understand.
I’ve been a geneticist for a long time. What genes have substations? What are substations in the context of a gene?
You still haven’t done a speck of math. If it’s obvious to you, you should be able to explain it in your own words.
Nor was it intended to, It was only intended to show that Behe’s model has no relevance to reality.
Do you accept that Lynch succeeded in showing this?
And quoting people saying you are wrong is a very strange way to try prove you are correct.
Substations?? And what makes you think that the genes in the Howe diagram are “unique” and have “many new mutations”? You’re just making stuff up.
I’m guessing substation is auto-incorrection for substitution.
Bill, I’m having trouble getting this. How do we know if a particular gene is unique? What does it mean for a gene to be unique? If a gene is unique, what are you comparing it with to determine that it has many mutations?
can you give an example of a unique gene with many new mutations?
Hi Bill.
I think you have completely missed @Rumraket’s point (which is not too different from the point I made above).
His point is that Behe’s, Gauger’s, etc scenarios/models are “entirely hypothetical”, “deliberately restrictive”, “entirely imaginary” & “don’t appear to obtain in reality”.
This means that you have two options:
come up with convincing evidence that (all prior evidence to the contrary notwithstanding) their scenarios/models are realistic; or
come up with convincing new evidence that evolution is vewy vewy restricted, that does not rely on these unrealistic scenarios/models.
Developing a quick case of creative amnesia and waffling on about " specific examples" and “how you can show how a new functional gene with unique sequences can form given a process that initiates with random change” really doesn’t help your case.
Finding ‘limitations’ within “entirely hypothetical”, “deliberately restrictive”, “entirely imaginary” & otherwise blatantly unrealistic scenarios/models has no more “value” in “helping understand limits to scientific inquiry” than somebody writing a paper on the phylogeny of Elves in Tolkien’s Middle Earth.
Hi Bill,
If I am understanding the biologists in this thread, the model used in evolutionary biology incorporates observed ratios of deleterious vs. neutral vs. beneficial mutations.
Behe’s paper presented a model that misrepresented those ratios. Therefore Behe’s calculations are NOT based on pop gen models and empirical evidence to any meaningful extent.
This has been stated to you in various formulations by many people, yet you still seem not to have grasped it. Your failure to grasp this critical point has derailed the conversation into a long and unproductive series of expressions of frustration.
I am having trouble discerning what you are trying to accomplish in this thread. But I do wish you a healthful and prosperous new year.
Chris
Hi Chris
Can someone make a detailed supported argument that Lynch’s assumptions are more accurate then Behe’s? I honestly do not know and have not looked at all the supporting evidence. My sense is they may both be right depending on the animal type and the specific genes tolerance for variation.
In supporting an edge to evolution we see in both cases (Lynch’s and Behe"s) the math shows evolutionary variation inside genes to be very limited.
Hi Walter
What makes a gene or protein it codes for unique is its sequence, length and its exon pattern. If we just look at a protein length it can vary form 50 to 30000 amino acids in length. As far as sequence variation there are around 2000 super families. Even among the same gene in different animals there can be different amounts of substitution.
Between humans and bovine there are over 20 AA substitutions in cytochrome B where the sequences of smooth muscle actin are the same. You can go on uniprot and look at different proteins to get a feel for the variation of AA substitution and similarities.
What’s really funny is that you seem to think that answers the question. That you are so easily bamboozled when ID’ers string together a bunch of sciencey-sounding nonsense does not mean everyone else is so gullible.
BTW, can you explain how such a large number of functional variants could exist if Behe was correct in his claim that all transitional states between a gene and its descendants are deleterious? To my admittedly nonexpert eyes that seems highly improbable.
Can you show me where he makes this claim?
In the very paper you have been talking about throughout this discussion.
You’re missing the point, which is that Behe is misrepresenting Lynch’s ratios. Why would Behe do that?
@WalterKloover asked for “an example of a unique gene with many new mutations.” Why didn’t you bother to provide one, Bill?
How many functional variants are there of the MYH7 gene in humans, Bill? It’s one of the most functionally complex proteins known.
He didn’t ask for that. He very clearly asked for “an example of a unique gene with many new mutations.”
To expert eyes it is laughably false.
How many functional variants are there of human MYH7, for example?
Behe
Experimental studies contradict Lynch’s assumption of complete neutrality as a rule; the majority of amino acid substitutions decrease protein function.
He did not make the comment you are assigning to him.
My comment was probably misleading. I was referring to the assumptions he used in his model, which were exactly as I have presented them. Even if he recognizes these assumptions were not completely in line with reality (Lynch also acknowledged this regarding his own model, saying it led to a significant underestimate of the speed with which new genes would be fixed) the accuracy of Behe’s model depends on how closely its parameters reflect reality.
So even though he may have modeled a situation where every transitional form is deleterious while believing the true situation was that mostly every transitional form is deleterious, it matters not since the reality is that mostly every transitional form is neutral, which approximates Lynch’s model. Behe’s model is just a fantasy.
I think this depends on the gene and coded protein and specie we are talking about. Alpha actin or beta catenin in mammals would not support your claim where a beta lactamase in bacteria might.
If Michael Lynch is assuming all amino acid substitutions are neutral his model is not accurate for mammals or higher order vertebrates.