Genes arrangements are the set of genes that make up a specific species.
Genes can mutate. 30% of gene changes do not affect amino acid substitutions. There are also amino acid substitutions that do not change function.
Mutations happen to individuals in a population but often those mutations are eliminated from the population due to their deleterious nature or drift.
In order for a gene set to change due to mutation genes need to be lost or new genes need to be gained. This involves more then single nucleotide substitutions.
Yeah, I have no clue what this means. Can someone qualified please confirm that all individuals belonging to a species share some minimal set of genes shared by no individual outside of that species? If this is so, in what sense is “gene arrangement” anything other than a fancier way of saying “species”?
Cool. What about those that do?
Cool. What about all of the times they are not eliminated, then? Also, is that what drift is? I thought genetic drift was the fixation of neutral changes not explicitly favoured or disfavoured by selection.
How much more does this involve, exactly? And why, do you reckon, is this a problem in any way?
To answer this we would need the gene sets of all species to see if two different species such as dogs and wolves share the same gene set. The gene sets I have seen show species have different gene sets.
They mutate a functional gene until the gene most likely loses function.
Drift can refer either to loss or fixation. If they are not eliminated they can persist in parts of the population or become fixed.
A gene can be lost due to a mutation or a few mutations that eliminate the genes function. Gene gain is a much bigger challenge. The current hypothesis is a gene is duplicated and it then serendiptiously finds function.
The challenge is that functional sequence space (its ability to interact with other genes and form a new function) is a small subset of total sequence space so the odds of the duplicated gene finding new function is small.
So to be clear: Are you saying that dogs and wolves do not share even a single gene in common? And did you expect different species to have identical genomes/gene sets?
How often is “most likely”? And what about those that evolve a new function, and don’t lose it?
Can you show some math to demonstrate that this “challenge” is so large that all deer cannot share a common ancestor? Thanks in advance.
He has no numbers for any of the relevant factors. He has no data on what fraction of sequence space is functional. He has been given such data and explanations for it, but he always just ignores it and forgets it even exists.
He also can’t show what fraction of the novel genes found in different species actually also have novel functions. Most of the non-shared genes are just duplicates that have diverged since the time of their initial duplication. He has no data on what fraction of these might have acquired a new function. Bill seems to think it’s all of them. He never says, but always treats all of them as if they have novel functions.
All he has is that Behe & Snoke once created a model in which a duplicate gene evolving a novel function has to go through an imaginary series of hoops Behe himself admits, in the very same paper, is probably unrealistically restrictive.
Behe has one weakly generous assumption in the paper, that a duplicate has already gone to fixation, but then all the rest of his assumptions are deliberately highly restrictive. But watch Bill focus on that one weakly generous assumption as if it balances out, if not totally overwhelms the restrictive ones (which is what Bill clearly believes it does). It’s that one little breadcrumb Behe knew to toss in there so his sycophants can brainlessly invoke it with zero clue of how little a difference it makes compared to his much more restrictive assumptions, like the fact that the novel function requires two, or more, mutations each of which are individually strongly deleterious null-mutations that completely eradicate function for the gene.
Because of computing limitations, the values of 0.01–0.0001 used for the mutation rate v in the simulations presented following are much higher than the biologically realistic value of about 10−8 (Drake et al. [1998](https://onlinelibrary.wiley.com/doi/full/10.1110/ps.04802904#bib9)), and the values of 1–100 used here for ρ are lower than the value of a thousand or greater expected for biologically realistic situations (Walsh 1995). However, the fact that Figure 2 shows that the fraction (1 - ϕ) of compatible mutants in our simulations follows equation 2 very closely over a wide range of values for λ and ρ in populations that reproduce either deterministically or stochastically makes us more confident when we extrapolate the model to biologically realistic values of v andρ.
Did you over look this?
It’s in the prior claim of deleterious mutations. Post 881
Even more, he has no data on the degree of connectivity of the functional portion, which is the truly relevant bit. Most genes do not derive from random sequences.
I have no idea at this point what the gene arrangement between dogs and wolves look like. What we are missing is the data from wolves.
I expected some species to share the same gene arrangements. When I generated a Venn diagram of 3 different types of fruit flies I expected more overlap.
Not clear the conditions exist to evolve a new function.
If you agree from a the duplication of a functional gene to a new function takes on average 500 AA substitutions (trials) and 6 AA substitutions per site will preserve protein function it then would be exceedingly unlikely for a new function to form from gene duplication and divergence.
They use 10-8 for the equation used to produce figure 6, which is also the figure from which they derive all the seemingly prohibitive numbers. So no, did you?
I have no idea what you are trying to say. Let’s add back the context so you can remember what you’re being asked:
So to recap, if there’s purifying selection to retain the function of the gene, it will accumulate mutations that do not eradicate it’s function, until such a time as it discovers a new function. Right?
That is to say, if we were to compare the genomes of two porpoises and one sunflower, it would be impossible to determine which was the sunflower because they would have “the same gene arrangements.” Maybe not specifically for porpoises and sunflowers, but it would be the case for some other pairs of species.
I have no idea why a person would believe something so ludicrous. You continue to astonish.
Not sure why you doubt it. Your pal Mike Behe even wrote a book describing how the malaria parasite evolved a new function that makes it resistant to chloroquine.
I do not agree. Please show that those conditions actually pertain in real life, and then show us the calculations that demonstrate that this is “exceedingly unlikely.” TIA.
A lot of interesting data in this one. For example that some domestic dog breeds are different from each other (not only from the grey wolf cousin thought to be similar to their last common ancestor, from each other) by over 3.5 million SNVs, and also have numerous chromosomal differences.
Some dog breeds also have more copies of some genes than others.
Next up: Bill will deny the common ancestry of domestic dog because differences in chromosomes, large numbers of mutations, or gene duplications or losses are all impossible in his alternative reality.
We present multiple independent lines of evidence that distinguish the dingo genome from that of the domestic dog breeds. There are at least three large chromosomal differences between CanFam_DDS and CanFam3.1 in addition to the previously described chromosome 6 AMY2B copy number expansion in most breed dogs. These three inversions and the AMY2B duplication occur in different subsets of breeds, so it is unlikely that they are assembly errors. Furthermore, chromosome 26 has a unique inversion in the Great Dane, showing that chromosomal rearrangements are found in domestic dogs. On average, we identified 21.78 Mb of large SVs in the dingo compared to breed dog reference genomes. In comparison, there are estimated to be 18.7 Mb of large variations in the average human genome (48).
Ye just spotted that too.
Millions of mutations separate different dog breeds. Yet in the new thread on Ewert’s dependency graph we are told that:
In contrast, the standard evolutionary framework provides no insight into how echolocation is implemented in different mammals. The commonly accepted evolutionary tree requires echolocation to have evolved independently three times as illustrated in Ewert (2023), Figure 1. Yet the maximum possible time for the evolution of a fully aquatic mammal or a bat is insufficient for more than two coordinated mutations to appear. Any evolutionary scenario for echolocation would require far more than two coordinated mutations (here ,here ), so evolution fails to explain this trait’s origin even once, let alone multiple times.
Just two “coordinated” mutations are impossible in millions of years they say. Just to be clear, a coodinated set of mutations is merely where the effect of one mutation depends on the presence of another mutation. So they are saying of the millions that have fixed in different dog breeds, not a single one could possibly have an epistatic interaction with another.
Now consider that the majority of mutations are known to have epistatic interactions, and that their fitness effects depend both on genetic background and environment.
That is not how the ID Creationists use the term, however. Which is not to say they use it in any consistent or coherent manner. But one of the references in the ENV article, predictably enough, is to Durrett and Schmidt (2008). This is how the authors describe what they are calculating: “In particular, we examine the waiting time for a pair of mutations, the first of which inactivates an existing transcription factor binding site and the second of which creates a new one.” And, while it is not clear from that sentence, they mean one specific pair of mutations, not just any pair that accomplishes that.
ID apologists regularly misrepresent that paper as demonstrating that it takes >100 million years for any two functional mutations to become fixed in the genome of an organism with a generation of time of 10 years or more.
I have discovered a new use for the concept of epistasis. Creationist Epistasis. It’s where the stupidity and falsehood of a creationist statement becomes apparent in the context of another creationist statement. Creationist statements always work in antagonistic form. It’s all always mutually refuting.
Defending creationism is also a form of anti-learning. The more creationist material you consume, the more confused and unable to make sense of biology you become. In fact, it’s loss-of-function learning. Encephalitic Entropy.
The subject is around gene arrangements which is comparing the types of genes the animals have. This paper does not discuss this.
We are not comparing genomes we are comparing genes.
These are examples of trivial changes not ones that we would assign to macro evolution.
What do you believe the conditions should be? Different versions of myosin are over 1000 amino acids separated in their sequence. How many searches were required for the original version of myosin to find a new function that is 1000 substitutions away?