snRNP公司
RNA剪接
生物
Prp24型
RNA结合蛋白
细胞生物学
SR蛋白
蛋白质剪接
小核RNA
德隆
小核核糖核蛋白
剪接体
酿酒酵母
核糖核蛋白
选择性拼接
遗传学
核糖核酸
信使核糖核酸
酵母
基因
泛素连接酶
非编码RNA
泛素
作者
Subbaiah Chalivendra,Shasha Shi,Xueni Li,Zhiling Kuang,Joseph GIovinazzo,Lingdi Zhang,John M. Rossi,Jingxin Wang,Anthony J. Saviola,Robb Welty,Shiheng Liu,Katherine F. Vaeth,Z. Hong Zhou,Kirk C. Hansen,J. Matthew Taliaferro,Rui Zhao
出处
期刊:RNA
[Cold Spring Harbor Laboratory Press]
日期:2024-04-30
卷期号:30 (8): 1070-1088
被引量:3
标识
DOI:10.1261/rna.079917.123
摘要
The recognition of the 5' splice site (5' ss) is one of the earliest steps of pre-mRNA splicing. To better understand, the mechanism and regulation of 5' ss recognition, we selectively humanized components of the yeast U1 (yU1) snRNP to reveal the function of these components in 5' ss recognition and splicing. We targeted U1C and Luc7, two proteins that interact with and stabilize the yU1 snRNA and the 5' ss RNA duplex. We replaced the zinc-finger (ZnF) domain of yeast U1C (yU1C) with its human counterpart, which resulted in a cold-sensitive growth phenotype and moderate splicing defects. We next added an auxin-inducible degron to yeast Luc7 (yLuc7) protein (to mimic the lack of Luc7Ls in human U1 snRNP). We found that Luc7-depleted yU1 snRNP resulted in the concomitant loss of Prp40 and Snu71 (two other essential yU1 snRNP proteins), and further biochemical analyses suggest a model of how these three proteins interact with each other in the U1 snRNP. The loss of these proteins resulted in a significant growth retardation accompanied by a global suppression of pre-mRNA splicing. The splicing suppression led to mitochondrial dysfunction as revealed by a release of Fe
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