Essential and recurrent roles for hairpin RNAs in silencing de novo sex chromosome conflict in Drosophila simulans
Fig 7
Summary of intrinsic and recurrent sex chromosome conflicts and their suppression by endogenous RNAi.
(Top) Wild-type individuals harboring intragenomic conflict systems typically exist in a cryptic state, in which de novo sex-linked meiotic drive loci are silenced posttranscriptionally by autosomal hpRNA loci that generate endogenous siRNAs. Their existence of meiotic drivers is hidden in this state, since animals have normal reproductive performance, even though there can be numerous X-linked drive loci (e.g., Dox/MDox/PDox1/PDox2 in D. simulans). (Middle) The deleterious activities of meiotic drive loci are unleashed upon mutation of the hpRNA suppressors (e.g., Tmy and Nmy). In D. simulans males, loss of nmy results in near-complete absence of male progeny, whereas loss of tmy causes complete sterility. Genetic interaction tests show that Tmy protects against sex ratio drive, but evidently in the contemporary derepressed state, X-linked drivers likely off-target to the X or autosome yielding absence of female gametes as well. (Bottom) We can infer that Dox family meiotic drives are selfish, rather than contributing to normal reproduction, since removal of all of these loci restores normal fertility and sex balance to hpRNA mutants. In a sense, this returns D. simulans to a D. melanogaster-like state, which lacks the Nmy/Tmy hpRNAs as well as all X-linked Dox family genes. hpRNA, hairpin RNA; siRNA, small interfering RNA.