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突变分析确定了酿酒酵母中端粒沉默所必需的RAP1的C末端尾巴结构域。

Mutational analysis defines a C-terminal tail domain of RAP1 essential for Telomeric silencing in Saccharomyces cerevisiae.

作者信息

Liu C, Mao X, Lustig A J

机构信息

Graduate Program in Molecular Biology, Cornell University Graduate School of Medical Sciences, New York, New York 10021.

出版信息

Genetics. 1994 Dec;138(4):1025-40. doi: 10.1093/genetics/138.4.1025.

Abstract

Alleles specifically defective in telomeric silencing were generated by in vitro mutagenesis of the yeast RAP1 gene. The most severe phenotypes occur with three mutations in the C-terminal 28 amino acids. Two of the alleles are nonsense mutations resulting in truncated repressor/activator protein 1 (RAP1) species lacking the C-terminal 25-28 amino acids; the third allele is a missense mutation within this region. These alleles define a novel 28-amino acid region, termed the C-terminal tail domain, that is essential for telomeric and HML silencing. Using site-directed mutagenesis, an 8-amino acid region (amino acids 818-825) that is essential for telomeric silencing has been localized within this domain. Further characterization of these alleles has indicated that the C-terminal tail domain also plays a role in telomere size control. The function of the C-terminal tail in telomere maintenance is not mediated through the RAP1 interacting factor RIF1: rap1 alleles defective in both the C-terminal tail and RIF1 interaction domains have additive effects on telomere length. Overproduction of SIR3, a dose-dependent enhancer of telomeric silencing, suppresses the telomeric silencing, but not length, phenotypes of a subset of C-terminal tail alleles. In contrast, an allele that truncates the terminal 28 amino acids of RAP1 is refractory to SIR3 overproduction. These results indicate that the C-terminal tail domain is required for SIR3-dependent enhancement of telomeric silencing. These data also suggest a distinct set of C-terminal requirements for telomere size control and telomeric silencing.

摘要

通过对酵母RAP1基因进行体外诱变,产生了在端粒沉默中特异性缺陷的等位基因。最严重的表型出现在C末端28个氨基酸的三个突变中。其中两个等位基因是无义突变,导致截短的阻遏物/激活蛋白1(RAP1)物种缺乏C末端的25 - 28个氨基酸;第三个等位基因是该区域内的错义突变。这些等位基因定义了一个新的28个氨基酸的区域,称为C末端尾巴结构域,它对端粒和HML沉默至关重要。利用定点诱变,已将对端粒沉默至关重要的一个8个氨基酸的区域(氨基酸818 - 825)定位在该结构域内。对这些等位基因的进一步表征表明,C末端尾巴结构域在端粒大小控制中也起作用。C末端尾巴在端粒维持中的功能不是通过RAP1相互作用因子RIF1介导的:在C末端尾巴和RIF1相互作用结构域均有缺陷的rap1等位基因对端粒长度具有累加效应。端粒沉默的剂量依赖性增强子SIR3的过量表达可抑制一部分C末端尾巴等位基因的端粒沉默表型,但不影响其长度表型。相比之下,一个截短RAP1末端28个氨基酸的等位基因对SIR3的过量表达具有抗性。这些结果表明,C末端尾巴结构域是SIR3依赖的端粒沉默增强所必需的。这些数据还表明,端粒大小控制和端粒沉默对C末端有一组不同的要求。

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