The closest things I can think of are caused by retrosposon events for X-encoded
genes which are metabolically necessary in post meiotic germ cells such as human
pyruvate dehydrogenase, PGK and MYCL2. However this is rather a specialized case as
the intronless genes are testis specific in expression and the gene with introns are
ubiquitously expressed. The intronless variant of pyruvate dehydrogenase appeared
after marsupials in evolution hence, they have only the intron containing copy while
eutherian mammals have both a intron containing version and an intronless version.
A parallel situation exists in the PKD1 gene which has 46 exon in human and 52 in
fugu caused by the loss of several intron in human to produce some very large exons
for example exon 15 is 3.6 kb in humans but the equivalent region is encoded by 5
exons the largest of which is 2.6 kb
Hope this helps
Jim
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