Abstract
An analysis of human exonic splicing elements in duplicated genes reveals their important role in the generation of new gene structures.
Highlights
The origin of new genes and their contribution to functional novelty has been the subject of considerable interest
Using the synonymous substitution rate (Ks) between duplicates as a proxy for time after gene duplication, we find that exonic splicing enhancer (ESE) and exonic splicing silencer (ESS) diverge with evolutionary time and the patterns are different between real and control motifs, indicating the effect of splicing
ESE and ESS divergences increase with evolutionary time after gene duplication The relative difference of ESE and ESS density between two paralogous exons increases as Ks becomes large (Figure 1a, b)
Summary
The origin of new genes and their contribution to functional novelty has been the subject of considerable interest. We examine a novel way that new gene structures could originate, namely through the evolution of new alternative splicing isoforms after gene duplication. It is possible that new gene structures are generated by the evolution of new alternative splicing forms after gene duplication. Consistent with this idea, 6 to 8% of profiled human-chimpanzee orthologous exons display significant splicing level differences in corresponding tissues. These genes affect diverse functions, including regulation of gene expression, signal transduction, cell death, immune defense, and susceptibility to diseases [5]. The details of this mechanism of alternative splicing evolution and its contributions to the evolution of new gene structures remain largely unknown
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