Don't bother. The situation in the LGLO gene is entirely different than what they are looking at in the Nature paper.
The mechanism of how an organism deletes a repeat(s) of a DNA segment as described in the paper is irrelevant to the type of mutations found in shared pseudogenes.
This pretty much sums it all up. Don;t look at data, don't think., circle wagons, contimue to parrot nonsense polemic about the mythical "LGLO gene".
The mechanism of how an organism deletes a repeat(s) of a DNA segment as described in the paper is irrelevant to the type of mutations found in shared pseudogenes.
Again, typical. Irrelevant? It's the most relevant study to date done to allow an understanding of chromosomal properties over an evolutionary time frame ever.
None of it is irrelevant to such discussions. The note to itchy and scratchy was concerning his spamming of a poor talk origins religious tract concerning repeat elements as an indicator of common descent.
As far as the "LGLO gene" perhaps you could actually describe it -- especialy in terms of the actual name of the gene, and the nature of the morphism in human, gorrilla and chimp.
In other words do something that is rather obviously becoming clear that is anathama to you -- think it through.
Or you could for the 14 thousandth time be one who monotonically repeats the holy writ about "exact same place" etc...
I know you won't understand this, but please read it:
L-Gulono-gamma-lactone oxidase (GULO), which catalyzes the last step of ascorbic acid biosynthesis, is missing in humans. The whole structure of the human gene homologue for this enzyme was disclosed by a computer-assisted search. Only five exons, as compared to 12 exons constituting the functional rat GULO gene, remain in the human genome. A comparison of these exons with those of their functional counterparts in rat showed that there are two single nucleotide deletions, one triple nucleotide deletion, and one single nucleotide insertion in the human sequence. When compared in terms of codons, the human sequence has a deletion of a single amino acid, two stop codons, and two aberrant codons missing one nucleotide besides many amino acid substitutions. A comparison of the remaining human exon sequences with the corresponding sequences of the guinea pig nonfunctional GULO gene revealed that the same substitutions from rats to both species occurred at a large number of nucleotide positions. From analyses of the molecular evolution of Alu sequences in the human GULO gene homologue, it is thought that two Alu sequences were inserted in the vicinity of a presumed position of lost exon 11 during the same period as GULO lost its function. It is predicted that six LINE-1 sequences located in and near the gene homologue were inserted not during that period.