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SPT16/CDC68中的突变可抑制影响酿酒酵母启动子功能的顺式和反式作用突变。

Mutations in SPT16/CDC68 suppress cis- and trans-acting mutations that affect promoter function in Saccharomyces cerevisiae.

作者信息

Malone E A, Clark C D, Chiang A, Winston F

机构信息

Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115.

出版信息

Mol Cell Biol. 1991 Nov;11(11):5710-7. doi: 10.1128/mcb.11.11.5710-5717.1991.

Abstract

SPT16 was previously identified as a high-copy-number suppressor of delta insertion mutations in the 5' regions of the HIS4 and LYS2 genes of Saccharomyces cerevisiae. We have constructed null mutations in the SPT16 gene and have demonstrated that it is essential for growth. Temperature-sensitive-lethality spt16 alleles have been isolated and shown to be pleiotropic; at a temperature permissive for growth, spt16 mutations suppress delta insertion mutations, a deletion of the SUC2 upstream activating sequence, and mutations in trans-acting genes required for both SUC2 and Ty expression. In addition, SPT16 is identical to CDC68, a gene previously shown to be required for passage through the cell cycle control point START. However, at least some transcriptional effects caused by spt16 mutations are independent of arrest at START. These results and those in the accompanying paper (A. Rowley, R. A. Singer, and G. C. Johnston, Mol. Cell. Biol. 11:5718-5726, 1991) indicate that SPT16/CDC68 is required for normal transcription of many loci in S. cerevisiae.

摘要

SPT16先前被鉴定为酿酒酵母HIS4和LYS2基因5'区域中δ插入突变的高拷贝数抑制因子。我们构建了SPT16基因的缺失突变体,并证明它对生长至关重要。已经分离出温度敏感致死性spt16等位基因,并显示其具有多效性;在允许生长的温度下,spt16突变抑制δ插入突变、SUC2上游激活序列的缺失以及SUC2和Ty表达所需的反式作用基因中的突变。此外,SPT16与CDC68相同,CDC68是先前显示通过细胞周期控制点START所必需的基因。然而,至少一些由spt16突变引起的转录效应与在START处的停滞无关。这些结果以及随附论文(A. Rowley、R. A. Singer和G. C. Johnston,《分子细胞生物学》11:5718 - 5726,1991)中的结果表明,SPT16/CDC68是酿酒酵母中许多基因座正常转录所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff4/361942/755146085f13/molcellb00035-0337-a.jpg

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