The MSL3 chromodomain directs a key targeting step for dosage compensation of the Drosophila

ABSTRACT: Active genes on the X chromosome of Drosophila males are upregulated by the Male-specific lethal (MSL) complex containing five MSL proteins and two non-coding roX RNAs. To probe the targeting mechanism, we have solved the structure of the MSL3 chromodomain, designed point mutations in key residues that disrupt putative methyl-lysine recognition, and tested their effect on full length MSL3 function. Transgenic males expressing these site-directed point mutants or MSL3short, a naturally occurring MSL3 form lacking the chromodomain, are unhealthy and developmentally delayed. Genomewide analyses of the binding patterns of these mutants support a two-step model: the first step is chromodomain-independent association with “chromatin entry sites” carrying GA-rich MSL recognition elements (MREs).

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Peter Park 

PROVIDER: E-GEOD-11817 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress