Your are still so shortsighted. Interdependence locks in one route out of many. You are still using the Sharpshooter fallacy.
Let’s use birds and bats as an example. Flight in birds requires flight feathers, and their actual forelimb isn’t that much different than our own in its overall shape. Flight in birds is dependent on feathers. Is that so for bats? No. They have a membrane stretched between their fingers. It shows that there is a different route for flight, one that isn’t dependent on feathers. The fitness landscape analogy really helps here, and you would benefit from understanding it.
I agree there can be multiple routes especially at the morphological level as you described. The issue is at the molecular level. If evolution starts building skin as a flight method a flight feather component like a keratin protein evolving is incompatible with this strategy. You are now restricted to skin cells once the process starts. As the process continues you are limited to functional constraints of what proceeded.
When you say Art’s article says something, and Art says his own article does not say what you say it does, why on earth would anyone believe you over Art?
. To give the reader a sense of the higher end (10^-10) of this range, it helps to keep in mind that 1000 liters of a typical pond will likely contain some 10^12 bacterial cells of various sorts. If each cell gives rise to just one new protein-coding region or variant (by any of a number of processes) in the course of several thousands of generations, then the probability of occurrence of a function that occurs once in every 10^10 random sequences is going to be pretty nearly 1. In other words, 1 in 10^-10 is a pretty large number when it comes to “probabilities” in the biosphere.
There seems to be some confusion regarding which article you are even trying to discuss. But, yes, those numbers are pretty conclusive, and it doesn’t require much complicated math at all. How many liters of water do you think there are in the biosphere?
I mean, is that seriously the passage you are claiming supports your position? If so, are you saying that Art is wrong in some of his parameters (e.g. the number of bacteria per volume of pond water, or frequency with which new protein coding regions will arise)? Or are you saying the numbers he uses in his estimation lead to the calculation that an event with probability 1 in 10^-10 will not realistically happen? It is not at all clear what you are disputing here.
What is required to get 10^10 trials in a bacteria fixed in the population of 10^12 bacteria? Start with the first fixed mutation. The fixation rate is 1/2N for neutral mutations. Since there are 10^12 bacteria mutating the theory says that the mutation rate equals the fixation rate. What is the mutation rate of bacteria? How long will it take to get 10^10 trials fixed in the population?
It’s the same thing at the molecular level. All of the concepts and pathways are exactly the same.
Let’s take something simple like a proteolytic cleavage site. It requires a recognition site in the protein that needs to be cleaved and a protease that binds to and cuts that sequence. They are dependent. However, there are many, many routes that this process can take. There can be different recognition sites, and different proteases that bind to it. However, once the interaction of two proteins results in a beneficial phenotype then both the recognition site and the protease that cuts at that site get their features locked in. That pathway is put in cement, especially when more proteins start interacting with those two initial proteins.
Take the problem to Larry Moran. See what he thinks. 1/n2 is probability of a neutral single mutation getting fixed in the population. Where n is the population.
He thinks the rate of fixation of neutral alleles should be neglible, despite the fact that it has been shown that the rate of fixation is equal to the rate of mutation. Which means roughly (for example) 100 neutral mutations are fixed in the human population every generation.
A general observation: It seems to me that part of the problem here is that people are attempting high level scientific discussion with @colewd, but Bill does not even understand the bare basics of what is being discussed, and is just very confused about evolution in general. He suddenly starts talking about fixation just above, apropos of nothing. Is he under the impression that a mutation must undergo fixation before it can be subject to further mutations in the process of evolving a new functional protein? Is that part of why he is unable to grasp the explanations he is receiving? If so, who know what other basic principles he is totally misunderstanding, but which the scientifically informed members are assuming he understands, because they are so basic?
Even if that was what he thinks, I don’t see how it would lead to the conclusion he draws, assuming his conclusions are logically based on the premises he accepts.