Epigenetic spreading of the Drosophila dosage compensation complex from roX RNA genes into flanking chromatin
Epigenetic spreading of the Drosophila dosage compensation complex from roX RNA genes into flanking chromatin
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DOI：
10.1016/s0092-8674(00)81979-0
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发表时间：
1999-08-20
期刊：
影响因子：
64.5
通讯作者：
Kuroda, MI
中科院分区：
文献类型：
--
作者：
Kelley, RL;Meller, VH;Kuroda, MI
多亚基的MSL剂量补偿复合物与果蝇单条雄性X染色体上的数百个位点结合，介导其高转录。雄性X染色体还覆盖有非编码的roX RNA。当msl3、mle或mof发生突变时，一种部分的MSL复合物仅结合在沿X染色体分布的大约35个异常位点上。我们表明其中两个位点是roX1和roX2基因，并推测它们的功能之一是为MSL复合物提供识别X染色体的进入位点。roX1基因即使被移到常染色体上，也为MSL复合物广泛扩散到侧翼染色质提供了一个成核位点。这种扩散可以在配对同源染色体之间顺式或反式发生。我们提出了一个关于剂量补偿复合物如何识别X染色质的模型。
The multisubunit MSL dosage compensation complex binds to hundreds of sites along the Drosophila single male X chromosome, mediating its hypertranscription, The male X chromosome is also coated with noncoding roX RNAs. When either msl3, mle, or mof is mutant, a partial MSL complex is bound at only similar to 35 unusual sites distributed along the X, We show that two of these sites are the roX1 and roX2 genes and postulate that one of their functions is to provide entry sites for the MSL complex to recognize the X chromosome. The roX1 gene provides a nucleation site for extensive spreading of the MSL complex into flanking chromatin even when moved to an autosome. The spreading can occur in cis or in trans between paired homologs. We present a model for how the dosage compensation complex recognizes X chromatin.