期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 402, 期 4, 页码 699-704出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.10.088
关键词
Dosage compensation; Epigenetics; MSL complex; Transcription
资金
- Royal Society of New Zealand [MAU204]
The male specific lethal (MSL) complex is required for X chromosome dosage compensation in Drosophila The complex binds to most actively transcribed X-linked genes in males and upregulates expression High resolution chromatin immunoprecipitation assays have identified over one hundred high affinity binding sites on the X chromosome One of the first high affinity sites discovered is at cytological location 18D11 The MSL complex binds weakly to a single copy of a 510 bp fragment from 18D11 but strongly to a tetramer of the fragment Here we have investigated the effect of insertion of sites of differing affinities either upstream or within the transcribed gene on complex binding and transcription upregulation Insertion of four copies of the 18D11 fragment upstream or at the 3' end of a reporter gene led to strong MSL complex binding and increased expression in males In contrast the MSL complex did not bind consistently to autosomal transgenes that contained a single copy of the 18D11 site upstream of the gene promoter However MSL complex binding was observed in all lines if the single 18D11 fragment was inserted into the 3' end of the reporter gene in either orientation This is consistent with previous studies that showed gene transcription facilitates MSL complex binding Surprisingly transcription elevation in males was only observed if the 18D11 fragment was in the forward orientation and only in some lines Our results suggest that MSL complex binding to weaker sites and transcription enhancement is influenced by gene transcription binding site orientation and the local chromatin environment In contrast strong binding sites do not need to be transcribed to recruit sufficient complex to cause transcription elevation of nearby genes (C) 2010 Elsevier Inc All rights reserved
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据