Don’t lie.
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Bill doesn’t lie. He just has very little control over what he types. He quite literally doesn’t know what he’s saying.
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I think you need to look more carefully at what the evolutionists are claiming. If specific functions are needed in biology then sequence matters and the ID argument wins.
The problem is the ID argument is based on how biology works and the evolutionists argument is not.
The evolutionists need to find a mechanism that explains the origin of new genes through reproduction or the single origin model will fail.
If you read carefully the sand walk article you cited you will see what is not explained is 700 genes in humans that are not found in chimps.
Improve your reading skills:
Much of the difference is due to insertion and deletion of members of gene families. One study shows that the human genome has 689 genes not present in the chimp genome and chimps have 729 genes not present in humans [Mammalian Gene Families: Humans and Chimps Differ by 6%]. That’s a total of 1,418 complete genes that are only found in one of the species.
At first glance this looks like 689 completely new genes have evolved in the human lineage since it diverged from our common ancestor with chimpanzees but looks can be deceiving. These genes are members of gene families and all that’s happened is that 689 orthologous genes have
either arisen by duplication in the human lineage orbeen lost by deletion in the chimp lineage or 689 new parologous genes have been “born” by gene duplication (or some combination).
(Deletion of text in original)
Thanks for the correction. We now have gene Venn diagrams of all primates that are more current.
You have to stop making these incoherent statements. Do even you know what you meant by that sentence? I guarantee nobody else does. The rest of your post (of all your posts) is no better.
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Did you even notice that the correction invalidated your main point? Stop. Think.
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No, that’s not how logic works. The fact that allele ratios of populations change over time, and often times produce overt variants, and that populations split and speciate, and that the rate at which all of that happens matches up with the ages of paleontological finds, which in many cases could be predicted in advance, as could features of genomes before they are sequences, would all remain facts. Evolution as the only theory of biodiversity does not hinge upon functions not needing to be specific, or upon sequence mattering, nor is it under any threat merely if by some miracle it turned out to be so.
Meanwhile, Intelligent Design has all of its homework still ahead demonstrating that an intelligent agency could, would, or did produce life as we know it, even if by some miracle it turned out after all, despite all hitherto gathered evidence to the contrary, that specific functions are needed in biology and are only achievable by very specific sequences.
Again, no. First of all, these mechanisms have been thoroughly accounted for. Your “nuh-uh”-ing at all of them does nothing to change that it is so. But, even if they were not, that does not automatically make the single origin model inadequate. If that model continues to make accurate predictions, then it is a successful model. Period. Whether anybody anywhere understands every detail of it or not, is entirely immaterial.
This is like saying that the General Theory of Relativity fails unless and until a quantum theory of gravity can be devised, and we had better go back to navigating by the night sky because GPS satellites cannot be trusted until such progress is achieved. It’s ludicrous. The merits of a scientific model are not contingent upon how complete it is, but rather upon the ratio of the volume of data it can predict against the volume of input it needs to render such predictions. That’s it. That’s science. Everything else is something else.
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It did not at all if you look at the most modern take on this.
It’s incoherent to you as I am making a higher level statement that you cannot yet accept. The conclusion is based on the sequence problem which you try and fight against with the TSS claim.
Your counter argument to the sequence problem is guys like Behe are committing the TSS. The TSS claim is based on the any function will do hypothesis. If specific type of functions are required then sequence specificity becomes important. If sequence specificity becomes important then the sequence problem (an almost infinite number of arrangements) becomes a killer problem for current evolutionary mechanisms being able to build a new functioning gene.
This is why DNA jock came up with the TSS label to fight gpuccio’s information argument. The use of a label is political discourse to try to discount an argument and have people look the other way.
The argument had no basis in reality. Biology requires specification as different proteins must work together to perform specific functions. This is so basic it is amazing Jock got away with this nonsense.
How do you still not understand this? It isn’t a question of whether “any function will do,” it’s a question of whether many sequences can perform the same function, which is supported by research.
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OK, I’ll look. What is the most modern take, and why did you instead cite a source that directly contradicts your claim?
That too was incoherent. Please stop. Please think.
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Different sequences performing the same function does not address the issue. Its the number of sequences that can before the same function vs the total sequence space.
It’s also a question of whether we, after the fact, are focusing only on a specific function we happen to see rather than all the other functions we could have seen. Note Bill’s repeated confusion over what neutral evolution is about. Does he know that only 1/(2N) of neutral mutations ever become fixed? Unlikely.
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Now you’re starting to get it. Then can you refute the research which shows that specific functions are actually comparatively common throughout the sequence space? Over a year ago, you said that you would take some time to read at least the abstracts of all the papers I linked. I’m sure you’ve had enough time by now.
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“… that I cannot be bothered to even begin attempting to actually show that it is the case.”
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As it turns out, the ‘sequence problem’ and ‘waiting time problem’ are just two sides of the same coin. Every paper published on the ‘waiting time problem’ thus far has looked at the time until two (or more) pre-specified , coordinated mutations become fixed in a population. But there are many ways to achieve a desired result in real biology, as all of the studies cited above show. So the waiting time ‘problem’ is a non-problem.
This comment is based one of your prior arguments based on your link.
The problem with your argument is biology requires specification as proteins need to work together. There may be several sequences that solve the problem but evidence is that this number is a tiny fraction of total sequence space. This causes the need for a mutational search which takes time. Proteins also need to perform different functions and that requires different proteins with different structures. Three of the muscle proteins actin, myosis and titin have different structures that must be compatible enough to work together.
If this search becomes successful then the waiting time problem is this change becoming fixed in the population.
Also your argument is based on Axe’s experiment. The experiment is based on bacteria and a single enzyme substrate. The problem gets much worse with multicellular eukaryotes.
There is no sequence problem until you demonstrate it mathematically. And since you can’t do math, there is no problem. When you insist there is in the face of reason, you are lying.
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The mathematics of the sequence problem n^p where p is the length of the sequence and n is the number of possible elements in each position. This calculation gets you the total sequence space. The sequence problem is the number of possible solutions is smaller than the total sequence space and most likely orders of magnitude smaller give the empirical data.
If the functional sequence space is smaller than the total sequence space what happens when you randomly change the sequence? Take your telephone and put a friends number down and randomly change it and see if anyone you know answers the phone to test this. How many changes on average would you fail to call one of your friends?
Now imagine if your various friends phone numbers were 500 digits long. How many friends would you need to have a reasonable chance of phoning a friend after changing 5% (25) of the numbers starting from a known friends number?
Like phone numbers protein sequences have working sequences and non working sequences. When they are long as 500 AA long (average human protein) the total possible arrangements are enormous.
You don’t see this as a challenge to evolutionary theory?
That’s a claim, not a demonstration. And in any event, the size of the sequence space is irrelevant, only the functional fraction.
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All you did was reassert the very thing we are disputing, without addressing the research that refutes it.
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