Indel driven rapid evolution of core nuclear pore protein gene promoters

Nuclear pore proteins (Nups) prominently are among the few genes linked to speciation from hybrid incompatibility in Drosophila. These studies have focused on coding sequence evolution of Nup96 and Nup160 and shown evidence of positive selection driving nucleoporin evolution. Intriguingly, channel Nup54 functionality is required for neuronal wiring underlying the female post-mating response induced by male-derived sex-peptide. A region of rapid evolution in the core promoter of Nup54 suggests a critical role for general transcriptional regulatory elements at the onset of speciation, but whether this is a general feature of Nup genes has not been determined. Consistent with findings for Nup54, additional channel Nup58 and Nup62 promoters also rapidly accumulate insertions/deletions (indels). Comprehensive examination of Nup upstream regions reveals that core Nup complex gene promoters accumulate indels rapidly. Since changes in promoters can drive changes in expression, these results indicate an evolutionary mechanism driven by indel accumulation in core Nup promoters. Compensation of such gene expression changes could lead to altered neuronal wiring, rapid fixation of traits caused by promoter changes and subsequently the rise of new species. Hence, the nuclear pore complex may act as a nexus for species-specific changes via nucleo-cytoplasmic transport regulated gene expression.

Automated summary

Nuclear pore proteins (Nups) have been identified as genes involved in speciation from hybrid incompatibility in Drosophila. Positive selection has been observed in the evolution of Nup96 and Nup160 coding sequences, suggesting their role in nucleoporin evolution. The functionality of channel protein Nup54 is crucial for the female post-mating response, and rapid evolution in its core promoter region indicates the importance of transcriptional regulatory elements in speciation. Rapid accumulation of insertions/deletions (indels) is also observed in the promoters of Nup58 and Nup62, suggesting an evolutionary mechanism driven by indel accumulation in core Nup promoters.