I'm deferring to
ERV's Opinion:
ERV:
No yay! Cause IRGM isnt the same IRGM that we had 50 million years ago. Its now got an ERV LTR for a promoter, it sits in a different part of the genome, and its surrounding genome landscape has changed dramatically-- 33 retrotransposons (LINES/SINES/LTRs) have taken up residence upstream of IRGM!! Some people have a 20,000 base-pair deletion upstream from IRGM. This leads to expression of IRGM in wrong tissues at wrong levels, which could be a potential cause of Crohns disease
She is flat out wrong. IRGM is an important regulator of autophagy and disregulation of this gene is speculated to be associated with Crohn's disease. SNPs and deletions upstream of this gene (near the transcription site) are associated with Crohn's disease. Read for yourself.
McCarroll, S. A. et al. Deletion polymorphism upstream of IRGM associated with altered IRGM expression and Crohn's disease. Nature Genet. 40: 1107-1112, 2008.
Perhaps you didn't read their analysis?
Perhaps you are just unaware of the difference between the structure of a gene and the structure of the protein after processing. Perhaps you don't know the difference between an intron and an exon and alternative splicing. The structure of the gene changed, yes. Heck, the ERV9 insertion coincides with the transcription start signal. However after RNA splicing, the protein pretty much does what the IRGM protein does in mice. And dysfunctional IRGM genes (NOT PROTEINS) are associated with Crohn's disease. Got it?
But the copying mechanisms didn't keep the genes intact.
Ed Yong again:
The part of the gene coding for the protein was kept in tact. The transcription site was the part that was affected

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It perfectly demonstrates why FLE is nonsense. A random event restoring a gene to functionality that may actually do more harm than good.
The gene works fine. Dysfunctional IRGM genes are associated with Crohn's disease. From a FLE perspective, it makes sense that old genes can become functional again (junk DNA is an argument from ignorance) due to the inherent optimal properties of the genetic code, the robustness of mutation induction and subsequent repair and viewing retroviral elements as vectors of optimization

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