This recent prepub found that the loss of the tail was (likely) largely mediated by a single Alu insertion:
tail-loss evolution was mediated by the insertion of an individual Alu element into the genome of the hominoid ancestor. We demonstrate that this Alu element – inserted into an intron of the TBXT gene (also called T or Brachyury10–12) – pairs with a neighboring ancestral Alu element encoded in the reverse genomic orientation and leads to a hominoid-specific alternative splicing event. To study the effect of this splicing event, we generated a mouse model that mimics the expression of human TBXT products by expressing both full-length and exon-skipped isoforms of the mouse TBXT ortholog. We found that mice with this genotype exhibit the complete absence of a tail or a shortened tail, supporting the notion that the exon-skipped transcript is sufficient to induce a tail-loss phenotype, albeit with incomplete penetrance. We further noted that mice homozygous for the exon-skipped isoforms exhibited embryonic spinal cord malformations, resembling a neural tube defect condition, which affects ∼1/1000 human neonates
You’re right, I missed that! If you’re reading this thread and you want to comment, please hop on to the other thread, which is now pretty well developed.
I greatly appreciate your enthusiastic moderation, @Dan_Eastwood ! Since my post is largely redundant alongside the OP of the other thread, I suggest just locking this thread and letting any discussion take place on the other. It will be easier for you, and I would avoid having to edit my post so it wouldn’t look like an out-of-place, redundant opening post in the middle of the other thread.
