We have argued that negative feedback regulation can decouple increases in gene copy number (via duplication) from an increase in the product of that gene and therefore equip genes with a duplicability advantage.
The current understanding of gene evolution via duplication suggests that duplicated genes could arise through different mechanisms including unequal crossing over (resulting in tandem duplication), retrotransposition, segmental duplication and chromosomal (or whole genome) duplication [ 42, 45].
In the present review, we have discussed genome evolution via duplication and the mechanisms involved in the fixation and maintenance of the duplicates.
Two or more genes within a given species that originated from a single parent gene via duplication events, usually with a subsequent, sometimes subtle, divergence of function.
In particular, these cells are thought to derive from a common ancestral cell via duplication (or furcation sensu Oakley et al. 2007) and divergence (making them "sister cell types"; Arendt 2003), with protostomes eventually using the rhabdomeric type in their eyes and deuterostomes using the ciliary type.
Vertebrate Apl1 has likewise clearly evolved via duplication from the more broadly distributed Apl2 (supplementary Figure S3).
Apparently, this subfamily evolved via duplication of one of the SPANX-N genes accompanied by deletion of the distal part of exon 2 (minisatellites) and rapid divergence.
Of these three groups, only primates have additionally evolved trichromatic color vision via duplication of the ancestral long-wavelength sensitive opsin, an event which occurred only 25 to 30 million years ago [39].
Fungi also contain both Apl1 and Apl2, but these form distinct phylogenetic clans (Figure S3), suggesting fungal Apl1 and Apl2 are paralogues that did not evolve via duplication in an early fungal lineage.
This protocoatomer hypothesis [18] is supported by the observation that vesicle coat proteins are well conserved across eukaryotes [65], [66], [67], [68] and have expanded via duplication and divergence [67], [69], [70].
The overall fold similarity between these two domains, together with the structural homology with other Kazal-type inhibitors, suggests that all Kazal-type inhibitors evolved from a common ancestral gene via duplication while maintaining divergent amino acid sequences.
