Here's a diagram that compares what is left of the human GULOP pseudogene with the functional gene in the rat genome.
Note the following features:
- The human pseudogene is missing the promoter and all of the regulatory sequences.
- The human pseudogene is missing exons I to VI.
- The human pseudogene is missing exon XI.
- There are several small deletions and in-frame stop codons in what is left of exons VII to X.
This isn't a problem for Jonathan McLatchie. Here's how it could happen.
As I mentioned previously, the GULO gene in humans is rendered inactive by multiple stop codons and indel mutations. These prevent the mRNA transcript of the gene from being translated into a functional protein. If the GULO gene really is functional in utero, therefore, presumably it would require that the gene's mRNA transcript undergo editing so that it can produce a functional protein. It's not at all difficult to understand how this could occur.Now there's a slight problem with this scenario since RNA editing requires RNA and, as far as I know, the human pseudogene isn't transcribed. Oh well, that's a minor quibble—I'm sure Jonathan McLatchie just forgot to explain how to get the transcript.
Editing of mRNA transcripts is a widely recognized phenomenon in biology today. The mRNA transcript would presumably need to have the stop codons replaced with amino-acid specifying codons (as well as other edits of course to correct frame shifts caused by indels). The occurrence of such a process is not unheard of. For instance, the transcripts of tRNA and rRNA genes typically undergo editing to render them functional. And the mRNAs for mitochondrial proteins (e.g. NADH dehydrogenase 7; cytochrome c oxidase III) in Trypanosoma brucei -- the parasite that causes sleeping sickness -- are known to undergo extensive editing, in many cases being substantially rewritten to produce functional transcripts (Ochsenreiter et al., 2008; Piller et al., 1996).
But there's another tiny flaw in his proposal. It's going to be a big challenge for RNA editing to create all those missing exons. I'm certain that Jonathan McLathie has thought about this. Maybe that part of the proposal was accidentally deleted from his post?
Here's the punchline, according to this IDiot.
If premature stop codons can be edited out of the mRNA transcript in this manner, thereby rendering functional what is otherwise a "pseudogene", this seems to me to have profound implications regarding not only GULO, but our understanding of pseudogenes in general.I look forward to the "fruitful research" that this "paradigm of design" will produce. If the IDiots actually discover an intelligent designer that can recreate missing exons in developing embryos (and then remove them in adults) then many of us are going to look very foolish.
If the hypothesis entertained here turns out to be correct, it will be yet another example of where a paradigm of design has led to fruitful scientific research. Of course, for ethical reasons, the hypothesis cannot be easily tested on humans. Guinea pigs also possess a GULO pseudogene with premature stop codons, however, and would make a good model organism for the testing of this hypothesis.
Jonathan McLatchie is very excited about the work being done by Intelligent Design Creationists and the new technologies that will prove intelligent design.
Given that:Do you still wonder why I call them "IDiots"?
It would seem that [scientists'] claim that the GULO pseudogene is a "silver bullet" argument for evolution is highly premature. An ID-based paradigm of biology can help us understand the functions of pseudogenes, whereas a neo-Darwinian paradigm leads us to wrongly assume these genes like the GULO "pseudogene" are "broken" genetic "junk."
- New technology suggests we're just standing on the shores of understanding a vast ocean of potentially functional pseudogenes,
- It's highly feasible to understand how this pseudogene might have function,
- Evidence suggests it might indeed have function during human development,