Dhh1p, a putative RNA helicase, associates with the general transcription factors Pop2p and Ccr4p from Saccharomyces cerevisiae.
Dhh1p, a putative RNA helicase, associates with the general transcription factors Pop2p and Ccr4p from Saccharomyces cerevisiae.
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DOI：
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发表时间：
1998-02
期刊：
影响因子：
3.3
通讯作者：
H. Hata;H. Mitsui;Hong Liu;Yongli Bai;C. Denis;Y. Shimizu;A. Sakai
中科院分区：
文献类型：
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作者：
H. Hata;H. Mitsui;Hong Liu;Yongli Bai;C. Denis;Y. Shimizu;A. Sakai
POP 2（Caf 1）蛋白在酿酒酵母中影响多种转录过程，并且是Ccr 4p复合物的组分。我们已经分离出5个pop 2缺失突变的多拷贝抑制基因：CCR 4、DHH 1（一种假定的RNA解旋酶）、PKC 1、STM 1和MPT 5（pop 2的多拷贝抑制基因）。CCR 4或DHH 1基因的过表达有效地抑制了与pop 2突变细胞相关的表型; PKC 1、STM 1或MPT 5基因的过表达仅产生部分抑制。CCR 4或DHH 1基因的破坏导致与在pop 2细胞中观察到的表型相似的表型。此外，DHH 1基因的过表达也抑制了ccr 4突变，表明POP 2、CCR 4和DHH 1基因之间存在密切关系。双杂交分析和免疫共沉淀实验表明，Pop 2 p和Dhh 1 p物理相互作用，这些和其他数据表明，Dhh 1 p也是Ccr 4p复合物的一个组成部分。最后，我们研究了与POP 2和PKC 1通路相关的因素之间的遗传相互作用。过表达PKC 1可抑制dhh 1或mpt 5细胞的温度敏感性生长缺陷，过表达Mpt 5可抑制mpk 1细胞的温度敏感性生长缺陷。这些结果和从POP 2和PKC 1途径的双突变体的表型分析表明，POP 2和PKC 1途径是独立的，但有一些重叠的功能。
The POP2 (Caf1) protein in Saccharomyces cerevisiae affects a variety of transcriptional processes and is a component of the Ccr4p complex. We have isolated five multicopy suppressor genes of a pop2 deletion mutation: CCR4, DHH1 (a putative RNA helicase), PKC1, STM1, and MPT5 (multicopy suppressor of pop two). Overexpression of either the CCR4 or DHH1 genes effectively suppressed phenotypes associated with pop2 mutant cells; overexpression of PKC1, STM1, or MPT5 genes produced only partial suppression. Disruption of the CCR4 or DHH1 genes resulted in phenotypes similar to those observed for pop2 cells. In addition, overexpression of the DHH1 gene also suppressed the ccr4 mutation, suggesting a close relationship between the POP2, CCR4, and DHH1 genes. Two-hybrid analysis and coimmunoprecipitation experiments revealed that Pop2p and Dhh1p interact physically, and these and other data suggest that Dhh1p is also a component of the Ccr4p complex. Finally, we investigated the genetic interaction between factors associated with POP2 and the PKC1 pathway. The temperature-sensitive growth defect of dhh1 or mpt5 cells was suppressed by overexpression of PKC1, and the defect of mpk1 cells was suppressed by overexpression of MPT5. These results and phenotypic analysis of double mutants from the POP2 and PKC1 pathways suggested that the POP2 and the PKC1 pathways are independent but have some overlapping functions.