首页> 外文期刊>Nucleic Acids Research >Saccharomyces cerevisiae HMO1 interacts with TFIID and participates in start site selection by RNA polymerase II
【24h】

Saccharomyces cerevisiae HMO1 interacts with TFIID and participates in start site selection by RNA polymerase II

机译:酿酒酵母HMO1与TFIID相互作用,并参与RNA聚合酶II的起始位点选择

获取原文
获取原文并翻译 | 示例
           

摘要

Saccharomyces cerevisiae HMO1, a high mobility group B ( HMGB) protein, associates with the rRNA locus and with the promoters of many ribosomal protein genes ( RPGs). Here, the Sos recruitment system was used to show that HMO1 interacts with TBP and the N-terminal domain ( TAND) of TAF1, which are integral components of TFIID. Biochemical studies revealed that HMO1 copurifies with TFIID and directly interacts with TBP but not with TAND. Deletion of HMO1 (Delta hmo1) causes a severe cold-sensitive growth defect and decreases transcription of some TAND-dependent genes. Dhmo1 also affects TFIID occupancy at some RPG promoters in a promoter-specific manner. Interestingly, over-expression of HMO1 delays colony formation of taf1 mutants lacking TAND (taf1 Delta TAND), but not of the wild-type strain, indicating a functional link between HMO1 and TAND. Furthermore, Delta hmo1 exhibits synthetic growth defects in some spt15 ( TBP) and toa1 (TFIIA) mutants while it rescues growth defects of some sua7 ( TFIIB) mutants. Importantly, Dhmo1 causes an upstream shift in transcriptional start sites of RPS5, RPS16A, RPL23B, RPL27B and RPL32, but not of RPS31, RPL10, TEF2 and ADH1, indicating that HMO1 may participate in start site selection of a subset of class II genes presumably via its interaction with TFIID.
机译:酿酒酵母HMO1是一种高迁移率B组(HMGB)蛋白,与rRNA基因座以及许多核糖体蛋白基因(RPG)的启动子相关。在这里,使用Sos募集系统显示HMO1与TFI和TAFID的组成部分TAF1的N末端域(TAND)相互作用。生化研究表明,HMO1与TFIID共纯化,并与TBP直接相互作用,但不与TAND相互作用。 HMO1(三角洲hmo1)的删除会导致严重的冷敏感的生长缺陷,并减少一些TAND依赖基因的转录。 Dhmo1还以启动子特异性方式影响某些RPG启动子的TFIID占用。有趣的是,HMO1的过表达延迟了缺乏TAND(taf1 Delta TAND)但不是野生型菌株的taf1突变体的菌落形成,表明HMO1和TAND之间存在功能联系。此外,Delta hmo1在某些spt15(TBP)和toa1(TFIIA)突变体中表现出合成的生长缺陷,而它可以挽救某些sua7(TFIIB)突变体的生长缺陷。重要的是,Dhmo1导致RPS5,RPS16A,RPL23B,RPL27B和RPL32的转录起始位点向上游移动,但不引起RPS31,RPL10,TEF2和ADH1的转录起始位点向上游移动,这表明HMO1可能参与了II类基因子集的起始位点选择。通过与TFIID的交互。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号