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酿酒酵母中一种参与DNA交联修复的可诱导基因SNM1的调控。

Regulation of SNM1, an inducible Saccharomyces cerevisiae gene required for repair of DNA cross-links.

作者信息

Wolter R, Siede W, Brendel M

机构信息

Institut für Mikrobiologie, Abt. Biologie für Mediziner, J.W. Goethe-Universität, Frankfurt am Main, FRG.

出版信息

Mol Gen Genet. 1996 Feb 5;250(2):162-8. doi: 10.1007/BF02174175.

Abstract

The interstrand cross-link repair gene SNM1 of Saccharomyces cerevisiae was examined for regulation in response to DNA-damaging agents. Induction of SNM1-lacZ fusions was detected in response to nitrogen mustard, cis-platinum (II) diamine dichloride, UV light, and 8-methoxypsoralen + UVA, but not after heat-shock treatment or incubation with 2-dimethylaminoethylchloride, methylmethane sulfonate or 4-nitroquinoline-N-oxide. The promoter of SNM1 contains a 15 bp motif, which shows homology to the DRE2 box of the RAD2 promoter. Similar motifs have been found in promoter regions of other damage-inducible DNA repair genes. Deletion of this motif results in loss of inducibility of SNM1. Also, a putative negative upstream regulation sequence was found to be responsible for repression of constitutive transcription of SNM1. Surprisingly, no inducibility of SNM1 was found after treatment with DNA-damaging agents in strains without an intact DUN1 gene, while regulation seems unchanged in sad1 mutants.

摘要

对酿酒酵母的链间交联修复基因SNM1进行了检测,以研究其对DNA损伤剂的反应调控。在氮芥、顺铂(II)二胺二氯化物、紫外线和8-甲氧基补骨脂素+紫外线A处理后,检测到SNM1-lacZ融合蛋白的诱导,但在热休克处理或与2-二甲基氨基乙基氯、甲基磺酸甲酯或4-硝基喹啉-N-氧化物孵育后未检测到。SNM1的启动子包含一个15bp的基序,与RAD2启动子的DRE2框具有同源性。在其他损伤诱导型DNA修复基因的启动子区域也发现了类似的基序。删除该基序会导致SNM1诱导性丧失。此外,发现一个假定的负上游调控序列负责抑制SNM1的组成型转录。令人惊讶的是,在没有完整DUN1基因的菌株中,用DNA损伤剂处理后未发现SNM1的诱导性,而在sad1突变体中调控似乎未改变。

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