3.3.2. Gene duplications
Body colour patterns and pigment cell types are more diverse in fishes than in any other vertebrate lineage, and it has been suggested that the evolution of this diversity was promoted by genome duplications, in particular a fish-specific genome duplication (FSGD) at the base of the teleost lineage, which increased the repertoire of genes potentially involved in pigmentation [39].
Following a duplication, species- or lineage-specific loss of gene duplicates, acquisition of novel functions by one paralog (neofunctionalisation) and the division of the original function between paralogs (subfunctionalisation) can contribute to the evolution of novel phenotypes. For example, tissue-specific expression of the paralogs can mitigate adverse pleiotropic effects of colour gene mutations on other traits [39], and life stage-specific expression of paralogs [61] can allow a trait to evolve even if its function in a particular life stage would otherwise constrain variation.
Indeed, whereas duplicated genes are typically lost from the genome at high rates, the majority of genes known to be involved in melanin and pteridine colour patterns have been retained in duplicate after the FSGD [39]. Duplicated colour genes cloned in cichlids include the receptor tyrosine kinase csf1r paralogs originating from the FSGD, of which the A paralog retained its function in cichlid pigmentation [29] whereas the B paralog may have functionally diverged [62]. Furthermore, one gene of the endothelin family, which expanded via whole genome duplications, is associated with cichlid colouration [55]. Surprisingly, none of the two cichlid-specific paralogs of a gene responsible for a zebrafish colour pattern mutant (ci-kir7) are expressed in the cichlid integument [63].