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与SAGA相关的Sgf73p在体内以依赖或不依赖组蛋白乙酰转移酶(HAT)的方式促进启动子处预起始复合物组装的形成。

SAGA-associated Sgf73p facilitates formation of the preinitiation complex assembly at the promoters either in a HAT-dependent or independent manner in vivo.

作者信息

Shukla Abhijit, Bajwa Pratibha, Bhaumik Sukesh R

机构信息

Department of Biochemistry and Molecular Biology, Southern Illinois University School of Medicine, Carbondale, IL-62901, USA.

出版信息

Nucleic Acids Res. 2006;34(21):6225-32. doi: 10.1093/nar/gkl844. Epub 2006 Nov 7.

Abstract

Although Sgf73p, a yeast homologue of human Sca7p, has recently been implicated as a new component of Spt-Ada-Gcn5-acetyltransferase (SAGA), its association with SAGA and functional role in regulation of transcription remain unknown in vivo. Here, using a chromatin immunoprecipitation (ChIP) assay, we show in vivo that, like SAGA, Sgf73p is recruited to the upstream activating sequence (UAS) of a SAGA-dependent gene, GAL1, in an activator-dependent manner. Further, Sgf73p is required for recruitment of SAGA to the GAL1 UAS, and facilitates formation of the preinitiation complex (PIC) assembly at the GAL1 promoter. When PIC is not formed in Deltasgf73, histone H3 is not evicted from the GAL1 promoter. Interestingly, PIC formation at GAL1 is not regulated by histone H3 acetylation or histone acetyltransferase (HAT) activity of SAGA. Similarly, Sgf73p facilitates PIC formation at another SAGA-dependent gene, ADH1, independent of histone H3 acetylation or HAT. In contrast, Sgf73p stimulates PIC formation at PHO84 (a SAGA-dependent gene), in a HAT-dependent-manner. Collectively, our data reveal that Sgf73p is required for SAGA recruitment, and stimulates PIC formation either in a HAT-dependent or -independent manner, providing significant information on how Sgf73p and possibly human Sca7p function physiologically.

摘要

尽管酵母中的Sgf73p是人类Sca7p的同源物,最近被认为是Spt-Ada-Gcn5-乙酰转移酶(SAGA)的一个新组分,但其在体内与SAGA的关联以及在转录调控中的功能作用仍不清楚。在这里,我们使用染色质免疫沉淀(ChIP)分析,在体内表明,与SAGA一样,Sgf73p以依赖激活因子的方式被募集到一个依赖SAGA的基因GAL1的上游激活序列(UAS)。此外,Sgf73p是SAGA被募集到GAL1 UAS所必需的,并促进在GAL1启动子处形成前起始复合物(PIC)。当在Deltasgf73中不形成PIC时,组蛋白H3不会从GAL1启动子上被驱逐。有趣的是,GAL1处的PIC形成不受组蛋白H3乙酰化或SAGA的组蛋白乙酰转移酶(HAT)活性的调节。同样,Sgf73p促进另一个依赖SAGA的基因ADH1处的PIC形成,与组蛋白H3乙酰化或HAT无关。相反,Sgf73p以依赖HAT的方式刺激PHO84(一个依赖SAGA的基因)处的PIC形成。总的来说,我们的数据表明Sgf73p是SAGA募集所必需的,并以依赖或不依赖HAT的方式刺激PIC形成,为Sgf73p以及可能的人类Sca7p的生理功能提供了重要信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25d0/1693896/8b81af9e4742/gkl844f1.jpg

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