Highly differentiated sex chromosomes create a lethal imbalance in gene expression in one sex. To accommodate hemizygosity of the X chromosome in male @entity238 , expression of X-linked genes increases twofold. This is achieved by the @entity3930 ( @entity3930 ) complex, which modifies chromatin to increase expression. Mutations that disrupt the X localization of this complex decrease the expression of X-linked genes and reduce male survival. The mechanism that restricts the @entity3930 complex to X chromatin is not understood. We recently reported that the siRNA pathway contributes to localization of the @entity3930 complex, raising questions about the source of the siRNAs involved. The X-linked 1.688 g/cm(3) satellite related repeats (1.688(X) repeats) are restricted to the X chromosome and produce small RNA, making them an attractive candidate. We tested RNA from these repeats for a role in dosage compensation and found that ectopic expression of single-stranded RNAs from 1.688(X) repeats enhanced the male lethality of mutants with defective X recognition. In contrast, expression of double-stranded hairpin RNA from a 1.688(X) repeat generated abundant siRNA and dramatically increased male survival. Consistent with improved survival, X localization of the @entity3930 complex was largely restored in these males. The striking distribution of 1.688(X) repeats, which are nearly exclusive to the X chromosome, suggests that these are cis-acting elements contributing to identification of X chromatin.

siRNAs from an X-linked satellite repeat promote X-chromosome recognition in XXXX .

@entity3930 :: ('MESH:D005834', 'Disease') :: ['MSL', 'male- specific lethal'] @entity238 :: ('7227', 'Species') :: ['fruit flies']
@entity238 :: (7227,Species) :: ['Drosophila melanogaster']
