Abstract
Segregation distortion refers to an unusual genetic phenomenon in diploid organisms by which the two alleles at a locus in a parent are not recovered in the classical 1:1 Mendelian ratio in its offspring. The Drosophila melanogaster neogene Sd was created by a duplication breakpoint on the left arm of chromosome 2 (2L), and encodes a truncated RanGAP protein with normal GTPase activity but which mis-localizes to the nucleus and disrupts Ran gradients. Male flies carrying Sd exhibit segregation distortion for the Rsp locus on the right arm of chromosome 2 (2R). Specifically, spermatids inheriting chromosome 2 with the Sd+ Rsps(s) genotype, in heterozygous males of genotype Sd Rspi/ Sd+ Rsps(s), fail to develop properly so that the majority of progeny (approaching 100%) carry just the Sd Rspichromosome. One recent paper reported novel RNAi-expressing transgenes with Sd-mimicking properties; and another reported localization of an X-linked suppressor which restores Mendelian transmission. This article highlights how Drosophila genetics resources made this possible, and the significance of these findings to nucleus-cytoplasm transactions of interest to the wider cell biology community.
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