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It has been argued that the evolution of novel functions in a new gene duplicate may be facilitated by radical changes in the exon-intron structure of the derived copy, typically manifest in structurally heterogeneous paralogs comprising partial and chimeric duplicates [ 3].
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However, due to the reduction of selective pressure on redundant gene copies in duplicated regions, duplicates may be lost or pseudogenized.
That is, in our framework duplicates may be originated by duplicated museum records, but also by data aggregators and by the spatial resolution of the environmental layers.
Hence, the high prevalence of complete duplication events within our data set of young human gene duplicates may be explained by human duplicons having lengthier tracts, although the role of purifying selection against shorter duplication tracts yielding partial and chimeric duplicates cannot be ruled out.
It has been reported that at least 20 percentof zebrafish genes are present in duplicate [27], and it is possible that a fraction of the duplicate copies might have been lost, or that some missing duplicates may be present in the genome but not yet discovered.
In plants, such duplicates may be due to polyploidy events.
These duplicates may be lost or be survival by either retaining their original functions, subfunctionalization or neofunctionalization.
Finally, IGF/CFTR duplicates may be linked with ATP1α1b/cldn10 on AS-23, which has homeologous affinities with AS-22.
Segmental duplicates may be more often retained due to subfunctionalisation, without increasing the likelihood of gene rearrangment.
Conversely, segmental duplicates may be more often retained due to subfunctionalization, without increasing the likelihood of gene rearrangment [ 77, 78].
We hypothesize that the higher number of duplicates may be associated with higher 11S globulin content in dicots.
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