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.
复制标题
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
中科院分区:
文献类型:
--
作者:
Gregory,SM;Sweder,KS
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.