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Does genetic conflict drive rapid molecular evolution of nuclear transport genes in Drosophila ?
Author(s) -
Presgraves Daven C.
Publication year - 2007
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.20555
Subject(s) - meiotic drive , ran , biology , genetics , drosophila melanogaster , gene duplication , heterochromatin , nuclear transport , locus (genetics) , gene , gtpase , nuclear gene , nucleoporin , microbiology and biotechnology , meiosis , cell nucleus , genome , chromatin
Abstract The Segregation Distorter ( SD ) system of Drosophila melanogaster is one the best‐characterized meiotic drive complexes known. SD gains an unfair transmission advantage through heterozygous SD/SD + males by incapacitating SD + ‐bearing spermatids so that virtually all progeny inherit SD . Segregation distorter ( Sd ), the primary distorting locus in the SD complex, is a truncated duplication of the RanGAP gene, a major regulator of the small GTPase Ran, which has several functions including the maintenance of the nucleocytoplasmic RanGTP concentration gradient that mediates nuclear transport. The truncated Sd‐RanGAP protein is enzymatically active but mislocalizes to the nucleus where it somehow causes distortion. Here I present data consistent with the idea that wild‐type RanGAP , and possibly other loci able to influence the RanGTP gradient, has been caught up in an ancient genetic conflict that predates the SD complex. The legacy of this conflict could include the unexpectedly rapid evolution of nuclear transport‐related proteins, the accumulation of chromosomal inversions, the recruitment of gene duplications, and the turnover of repetitive sequences in the centric heterochromatin. BioEssays 29:386–391, 2007. © 2007 Wiley Periodicals, Inc.