so we only need to deal with about no more than few convergent loss. now, take a look at this figure:
as you can see above, about 6 different exons loss are shared between marmoset and microbat, but surprisingly, without a common descent. this finding prove that we can get the same exon loss without a common descent. therefore a shared exon loss cant be evidence for a common descent.
(reference:
A “forward genomics” approach links genotype to phenotype using independent phenotypic losses among related species)
There are a number of things to say about this, so this is likely to be a longer post with some technical details. The major import of this post is that you have cited a paper and figure, which doesn't support your position. On the contrary, it demolishes it.
First, you need to understand that the process we are looking at occurs in more than one stage. Initially there is a mutation which prevents the gene from working - a loss of function mutation. Such a mutation could be a frame-shift indel, a substitution which produces a stop codon or some other fatal missense, a splice donor or acceptor site mutation and so forth. It is unlikely to be the loss of an entire exon. Once the pseudogene has fixed in the population and is no longer under selection, it is free to degrade through neutral drift, and that degrading over time leads to the accumulation of further mutations such as indels, substitutions, loss of exons and so on.
Wherever a mutation occurs before the divergence of two taxa, we expect to find that mutation in both taxa. Where the mutation occurs after the divergence it will be found only in one taxon and not the other. So, the degraded pseudogene itself forms a family tree, with closely related species sharing more of the accumulated mutations than is shared with less closely related taxa.
Look to the left hand side of the figure where you will see a phylogeny with the loss of GULO marked by crosses. The hypothesis is that guinea pigs, Haplorhini and two types of bats independently lost the GULO gene (four separate events). Those losses are marked by crosses. So the hypothesis is that that the GULO gene was lost once in the common ancestor of the Haplorhini and that is why all tarsiers, monkeys and apes lack the gene.
Now, since the Haplorhini form a family tree with the divergence of different populations within that group inferred from phenotypic and genetic data, we predict that the more closely related species will share more of the subsequently accumulated mutations than more distantly related species. What do we see?
Let's start with human and chimp, the most closely related great apes. The accumulated mutations are identical:
* Loss of exons 2, 3, 6 and 8 and partial loss of exon 11
* A frameshift deletion in exon 7
* Splice donor site mutation 5'wards of exon 7
* A frameshift insertion on exon 9
* Splice donor site mutation 5'wards of exon 9
* A frameshift deletion on exon 10
* A stop mutation on exon 12
Gorilla: The same except the additional deletion of four base pairs on exon 7 and seven base pairs on exon 9 which we can infer a gorilla specific mutations
Orangutan: The same apart from a splice donor mutation 5'wards of exon 5 not present in human, chimp or gorilla.
Rhesus monkey, an Old World monkey: Shows the same pattern apart from a 16bp deletion on exon 7
Marmoset, a New World monkey: The gene is more highly degraded than in any of the Catarrhini (Old World monkeys and apes). In addition to the above exon losses, it has lost exons 4, 5, 7 and 10; and exon 11, partly lost in the Catarrhini is completely lost in marmoset. In addition there a 2bp and a 38bp insertion on exon 9 and 5bp deletion on exon 12. However the pattern of a stop mutation on exon 10 and the splice donor mutation on exon 9 is the same, suggesting that these mutations pre-date the divergence of Catarrhini and new world monkeys.
Tarsier: Loss of exons 2, 3,and 6 in common with the simians, but different in many other respects, suggesting that the original loss of function occurred shortly before the divergence of tarsiers and monkeys.
So we can see that the prediction that more closely related species will have accumulated a more similar set of mutations on the pseudogene over time is very powerfully borne out and illustrated in this figure.
What about species that independently lost the GULO gene? It is clear that the pattern of degrading the pseudogene is unrelated to the Haplorhini. In guinea pig there are stop mutations on exons 2 and 3, which exons are not present in any of the Haplorhini. Likewise exons 8 and 11 are present in guinea pig and lost or partly lost in Haplorhini, there is a splice acceptor site mutation on exon 12 etc. The pattern of accumulated mutations in the two bat species shows no commonality with guinea pig, Haplorhini and one another.
So this figure is powerful evidence for common descent and the family tree of the monkeys and apes, showing the close relatedness of the great apes including man. Xianghua has to explain how come all the Haplorhini have a broken GULO gene and why the pattern of accumulated mutations is the same as the family tree of the clade. The accumulated mutations on the pseudogene of man and chimpanzee are identical, and of all the Catarhini almost identical and it is simply not reasonable to suggest that this occurred independently.
