A sequence motif within chromatin entry sites directs MSL establishment on the Drosophila X chromosome

被引:206
作者
Alekseyenko, Artyom A. [1 ,2 ]
Peng, Shouyong [1 ,3 ]
Larschan, Erica [1 ,2 ]
Gorchakov, Andrey A. [1 ,2 ]
Lee, Ok-Kyung [1 ]
Kharchenko, Peter [3 ]
McGrath, Sean D. [4 ,5 ]
Wang, Charlotte I. [2 ]
Mardis, Elaine R. [4 ,5 ]
Park, Peter J. [1 ,3 ]
Kuroda, Mitzi I. [1 ,2 ]
机构
[1] Brigham & Womens Hosp, Dept Med, Div Genet, Harvard Partners Ctr Genet & Genom, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA
[3] Childrens Hosp, Childrens Hosp Informat Program, Boston, MA 02115 USA
[4] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63108 USA
[5] Washington Univ, Sch Med, Genome Sequencing Ctr, St Louis, MO 63108 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1016/j.cell.2008.06.033
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The Drosophila MSL complex associates with active genes specifically on the male X chromosome to acetylate histone H4 at lysine 16 and increase expression approximately 2-fold. To date, no DNA sequence has been discovered to explain the specificity of MSL binding. We hypothesized that sequence-specific targeting occurs at "chromatin entry sites,'' but the majority of sites are sequence independent. Here we characterize 150 potential entry sites by ChIP-chip and ChIP-seq and discover a GA-rich MSL recognition element (MRE). The motif is only slightly enriched on the X chromosome (similar to 2fold), but this is doubled when considering its preferential location within or 30 to active genes (> 4-fold enrichment). When inserted on an autosome, a newly identified site can direct local MSL spreading to flanking active genes. These results provide strong evidence for both sequence-dependent and -independent steps in MSL targeting of dosage compensation to the male X chromosome.
引用
收藏
页码:599 / 609
页数:11
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