Local spreading of MSL complexes fromroXgenes on theDrosophilaX chromosome

Abstract

MSL proteins and noncodingroXRNAs form complexes to up-regulate hundreds of genes on theDrosophilamale X chromosome, and make X-linked gene expression equal in males and females. Altering the ratio of MSL proteins toroXRNA dramatically changes X-chromosome morphology. In protein excess, the MSL complex concentrates near sites ofroXtranscription and is depleted elsewhere. These results support a model for distribution of MSL complexes, in which local spreading incisfromroXgenes is balanced with diffusion of soluble complexes intrans. When overexpressed, MSL proteins can recognize the X chromosome, modify histones, and partially restore male viability even in the absence ofroXRNAs. Thus, the protein components can carry out all essential functions of dosage compensation, butroXRNAs facilitate the correct targeting of MSL complexes, in part by nucleation of spreading from their sites of synthesis.