Deletion of the CSB homolog, RAD26, yields Spt(-) strains with proficient transcription-coupled repair.

Deletion of the CSB homolog, RAD26, yields Spt(-) strains with proficient transcription-coupled repair.
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CSB 同源物 RAD26 的缺失产生具有熟练转录偶联修复的 Spt(-) 菌株。

DOI:
10.1093/nar/29.14.3080
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发表时间:
2001
影响因子:
14.9
通讯作者:
Sweder,KS
Sweder,KS
中科院分区:
生物学2区
文献类型:
--
作者:
Gregory,SM;Sweder,KS

文献摘要

被引文献

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先前已表明,酵母菌株 W303-1B 中 RAD26 的破坏会导致菌株缺乏转录偶联修复 (TCR),即表达基因的转录链相对于非转录链和基因组其余部分的优先修复。RAD26 编码与科凯恩综合征 B 组蛋白 (CSB) 同源的蛋白质,并且是 DNA 依赖性 SWI2/SNF2 家族的成员参与染色质重塑的 ATP 酶。与 therad26 突变体一样,科凯恩综合征患者的细胞在 TCR 方面也存在缺陷。我们通过破坏两个修复能力强的实验室菌株中的 RAD26 来检查 Rad26 在 TCR 中的作用,值得注意的是,没有观察到对 TCR 的影响。我们的结果表明单独破坏 RAD26 不足以损害 TCR。因此,W303-1B 必定已经具有突变,该突变与 RAD26 的破坏一起导致 TCR 缺陷。我们认为科凯恩综合征细胞中的其他基因发生突变,导致 TCR 缺陷。令人惊讶的是,RAD26 的缺失会导致基因表达受到侧翼转座子 δ 元件(一种 Spt 表型)的抑制。 δ 元素似乎会扰乱局部染色质结构。 rad26Δ 突变体中 δ 元件侧翼的基因表达与 Rad26 在染色质重塑中的作用一致。
It has been previously shown that disruption ofRAD26in yeast strain W303-1B results in a strain that is deficient in transcription-coupled repair (TCR), the preferential repair of the transcribed strand of an expressed gene over the non-transcribed strand and the rest of the genome.RAD26encodes a protein that is homologous to Cockayne syndrome group B protein (CSB) and is a member of the SWI2/SNF2 family of DNA-dependent ATPases involved in chromatin remodeling. Like therad26mutant, cells from Cockayne syndrome patients are defective in TCR. We examined the role of Rad26 in TCR by disruptingRAD26in two repair-proficient laboratory strains and, remarkably, observed no effect upon TCR. Our results indicate that disruption ofRAD26alone is insufficient to impair TCR. Thus, W303-1B must already possess a mutation that, together with disruption ofRAD26, causes a deficiency in TCR. We suggest that other genes are mutated in Cockayne syndrome cells that contribute to the deficiency in TCR. Surprisingly, deletion ofRAD26results in expression of genes that are repressed by flanking transposon δ elements, an Spt–phenotype. The δ elements appear to perturb local chromatin structure. Expression of genes flanked by δ elements inrad26Δ mutants is consistent with a role for Rad26 in chromatin remodeling.