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

Tuba H. Sural, Shouyong Peng, Bing Li, Jerry L. Workman, Peter J. Park, Mitzi I. Kuroda

Research output: Contribution to journalArticle

73 Scopus citations

Abstract

The male-specific lethal (MSL) complex upregulates the single male X chromosome to achieve dosage compensation in Drosophila melanogaster. We have proposed that MSL recognition of specific entry sites on the X is followed by local targeting of active genes marked by histone H3 trimethylation (H3K36me3). Here we analyze the role of the MSL3 chromodomain in the second targeting step. Using ChIP-chip analysis, we find that MSL3 chromodomain mutants retain binding to chromatin entry sites but show a clear disruption in the full pattern of MSL targeting in vivo, consistent with a loss of spreading. Furthermore, when compared to wild type, chromodomain mutants lack preferential affinity for nucleosomes containing H3K36me3 in vitro. Our results support a model in which activating complexes, similarly to their silencing counterparts, use the nucleosomal binding specificity of their respective chromodomains to spread from initiation sites to flanking chromatin.

Original languageEnglish (US)
Pages (from-to)1318-1325
Number of pages8
JournalNature Structural and Molecular Biology
Volume15
Issue number12
DOIs
StatePublished - Dec 1 2008

ASJC Scopus subject areas

  • Structural Biology
  • Molecular Biology

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