|Citation||Sural, T.H., Peng, S., Li, B., Workman, J.L., Park, P.J., Kuroda, M.I. (2008). The MSL3 chromodomain directs a key targeting step for dosage compensation of the Drosophila melanogaster X chromosome. Nat. Struct. Mol. Biol. 15(12): 1318--1325. (Export to RIS)|
|Publication Type||Research paper|
|PubMed 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.|
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|Language of Publication||English|
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|Abbreviation||Nat. Struct. Mol. Biol.|
|Title||Nature Structural and Molecular Biology|
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|Natural transposons (1)|