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


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2008-12

AUTHORS

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

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. More... »

PAGES

1318-1325

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nsmb.1520

DOI

http://dx.doi.org/10.1038/nsmb.1520

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1036614550

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19029895


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