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合成致死突变表明U5小核RNA与剪接第二步所需的四种蛋白质之间存在相互作用。

Synthetic lethal mutations suggest interactions between U5 small nuclear RNA and four proteins required for the second step of splicing.

作者信息

Frank D, Patterson B, Guthrie C

机构信息

Department of Biochemistry and Biophysics, University of California, San Francisco 94143.

出版信息

Mol Cell Biol. 1992 Nov;12(11):5197-205. doi: 10.1128/mcb.12.11.5197-5205.1992.

DOI:10.1128/mcb.12.11.5197-5205.1992
PMID:1406691
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC360453/
Abstract

To investigate the function of the U5 small nuclear ribonucleoprotein (snRNP) in pre-mRNA splicing, we have screened for factors that genetically interact with Saccharomyces cerevisiae U5 snRNA. We isolated trans-acting mutations that exacerbate the phenotypes of conditional alleles of the U5 snRNA and named these genes SLU, for synergistically lethal with U5 snRNA. SLU1 and SLU2 are essential for the first catalytic step of splicing, while SLU7 and SLU4 (an allele of PRP17 [U. Vijayraghavan, M. Company, and J. Abelson, Genes Dev. 3:1206-1216, 1989]) are required only for the second step of splicing. Furthermore, slu4-1 and slu7-1 are lethal in combination with mutations in PRP16 and PRP18, which also function in the second step, but not with mutations in factors required for the first catalytic step, such as PRP8 and PRP4. We infer from these data that SLU4, SLU7, PRP18, PRP16, and the U5 snRNA interact functionally and that a major role of the U5 snRNP is to coordinate a set of factors that are required for the completion of the second catalytic step of splicing.

摘要

为了研究U5小核核糖核蛋白(snRNP)在mRNA前体剪接中的功能,我们筛选了与酿酒酵母U5 snRNA发生遗传相互作用的因子。我们分离出了一些反式作用突变,这些突变会加剧U5 snRNA条件等位基因的表型,并将这些基因命名为SLU,即与U5 snRNA协同致死。SLU1和SLU2对于剪接的第一步催化至关重要,而SLU7和SLU4(PRP17的一个等位基因[U. Vijayraghavan、M. Company和J. Abelson,《基因与发育》3:1206 - 1216,1989])仅在剪接的第二步中需要。此外,slu4 - 1和slu7 - 1与PRP16和PRP18的突变组合是致死的,PRP16和PRP18也在第二步中起作用,但与第一步催化所需因子的突变(如PRP8和PRP4)组合则不会致死。我们从这些数据推断,SLU4、SLU7、PRP18、PRP16和U5 snRNA在功能上相互作用,并且U5 snRNP的主要作用是协调一组完成剪接第二步催化所需的因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a5b/360453/9daa0d086835/molcellb00134-0403-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a5b/360453/e93bf015bbfb/molcellb00134-0402-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a5b/360453/9daa0d086835/molcellb00134-0403-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a5b/360453/e93bf015bbfb/molcellb00134-0402-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a5b/360453/9daa0d086835/molcellb00134-0403-a.jpg

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本文引用的文献

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拟南芥环肽酶 CYP18-1 促进 PRP18 去磷酸化和热胁迫下内含子的剪接。
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