So a testable model of this transition should be easy. 
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That model is tested in the thread I linked.
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Show how you get from a common ancestors genome to a chimp population and a human population with the mechanisms of your choice.
Why has this never been done?
Through mutations. I fail to see why you have such a tough time understanding this simple concept.
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Chimp:AGGTGTCCGTAAATGA
Human:AGGTGACCGTAAATGAThe two sequences differ by a single letter, and the mechanism is mutation. What is so hard to understand?
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Ok you have looked at about .000001% of the genomes change. I guess that’s a good start
The problem you will run into as you improve your analysis is trying to explain the differences especially the ones that are functional and very different sequences. Pauls post highlights these issues.
What issues? Can you point to a single difference between the chimp and human genomes that is a problem?
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I get the play on words in the title, and it honestly is rather interesting to see an example of a pseudogene with a specific activity. There are also others, but showing an example of a single pseudogene doing something in a cell is a very long way from toppling the evidence of pseudogenes as an evolutionary “discard pile” at the genetic level.
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The functional sequences with low or no homology found in Pauls paper.
This is a legitimate criticism.
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Not only that, but pseudogenes only make up 5% of the human genome. Even if every pseudogene has function it does nothing to show that the majority of the human genome has function.
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Which of those functional sequences do not have homologs in the chimp and human genomes?
Wasn’t this discussed elsewhere on this site recently?
Are you thinking of this thread?
Recent de novo origin of human protein-coding genes
-Author Affiliations
- Smurfit Institute of Genetics, University of Dublin, Trinity College, Dublin 2, Ireland
Abstract
The origin of new genes is extremely important to evolutionary innovation. Most new genes arise from existing genes through duplication or recombination. The origin of new genes from noncoding DNA is extremely rare, and very few eukaryotic examples are known. We present evidence for the de novo origin of at least three human protein-coding genes since the divergence with chimp. Each of these genes has no protein-coding homologs in any other genome, but is supported by evidence from expression and, importantly, proteomics data. The absence of these genes in chimp and macaque cannot be explained by sequencing gaps or annotation error. High-quality sequence data indicate that these loci are noncoding DNA in other primates. Furthermore, chimp, gorilla, gibbon, and macaque share the same disabling sequence difference, supporting the inference that the ancestral sequence was noncoding over the alternative possibility of parallel gene inactivation in multiple primate lineages. The genes are not well characterized, but interestingly, one of them was first identified as an up-regulated gene in chronic lymphocytic leukemia. This is the first evidence for entirely novel human-specific protein-coding genes originating from ancestrally noncoding sequences. We estimate that 0.075% of human genes may have originated through this mechanism leading to a total expectation of 18 such cases in a genome of 24,000 protein-coding genes.
From the abstract:
There are DNA homologs.
If you do find orphan genes with no DNA homologs, please present the sequence and show us why known processes of mutation would not be able to produce them.
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Depends on how we define homolog.
It’s your claim that they can. I know your working hard to improve Dawkins Model
Yes that’s the one, tank you. Of the 56 human sequences that had below 50% similarity to the chimp genome, how much DNA are we talking about? How long are these sequences?
Beautiful figure, thanks for sharing this. It’s fascinating to see that (at least in this figure) the proportion of pseudogenes in the human genome is 5X larger than the proportion of exons!
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