@article {153031,
	title = {The MSL3 chromodomain directs a key targeting step for dosage compensation of the Drosophila melanogaster X chromosome.},
	journal = {Nat Struct Mol Biol},
	volume = {15},
	number = {12},
	year = {2008},
	month = {2008 Dec},
	pages = {1318-25},
	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.

},
	keywords = {Amino Acid Substitution, Animals, Animals, Genetically Modified, Drosophila melanogaster, Drosophila Proteins, Electrophoretic Mobility Shift Assay, Female, Histones, Male, Microarray Analysis, Models, Biological, Mutagenesis, Site-Directed, Mutant Proteins, Mutation, Missense, Nuclear Proteins, Protein Binding, Sequence Deletion, Transcription Factors, X Chromosome},
	issn = {1545-9985},
	doi = {10.1038/nsmb.1520},
	author = {Sural, Tuba H and <b>Peng, Shouyong</b> and Li, Bing and Workman, Jerry L and <b>Park, Peter J</b> and Kuroda, Mitzi I}
}
