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酵母rad6δ突变的DNA修复缺陷的交配型抑制需要RAD52上位性组中基因的活性。

Mating-type suppression of the DNA-repair defect of the yeast rad6 delta mutation requires the activity of genes in the RAD52 epistasis group.

作者信息

Yan Y X, Schiestl R H, Prakash L

机构信息

Department of Biophysics, University of Rochester School of Medicine, NY 14642, USA.

出版信息

Curr Genet. 1995 Jun;28(1):12-8. doi: 10.1007/BF00311876.

Abstract

The RAD6 gene of Saccharomyces cerevisiae is required for post-replication repair of UV-damaged DNA, UV mutagenesis, and sporulation. Here, we show that the radiation sensitivity of a MATa rad6 delta strain can be suppressed by the MAT alpha 2 gene carried on a multicopy plasmid. The a1-alpha 2 suppression is specific to the RAD6 pathway, as mutations in genes required for nucleotide excision repair or for recombinational repair do not show such mating-type suppression. The a1-alpha 2 suppression of the rad6 delta mutation requires the activity of the RAD52 group of genes, suggesting that suppression occurs by channelling of post-replication gaps present in the rad6 delta mutant into the RAD52 recombinational repair pathway. The a1-alpha 2 repressor could mediate this suppression via an enhancement in the expression, or the activity, of recombination genes.

摘要

酿酒酵母的RAD6基因是紫外线损伤DNA的复制后修复、紫外线诱变和孢子形成所必需的。在此,我们表明,携带在多拷贝质粒上的MATα2基因可以抑制MATa rad6δ菌株的辐射敏感性。a1-α2抑制作用对RAD6途径具有特异性,因为核苷酸切除修复或重组修复所需基因的突变并未表现出这种交配型抑制。rad6δ突变的a1-α2抑制作用需要RAD52基因家族的活性,这表明抑制作用是通过将rad6δ突变体中存在的复制后缺口导入RAD52重组修复途径而发生的。a1-α2阻遏物可以通过增强重组基因的表达或活性来介导这种抑制作用。

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