Deletion of the Saccharomyces cerevisiae gene RAD30 encoding an Escherichia coli DinB homolog confers UV radiation sensitivity and altered mutability.
Deletion of the Saccharomyces cerevisiae gene RAD30 encoding an Escherichia coli DinB homolog confers UV radiation sensitivity and altered mutability.
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编码大肠杆菌 DinB 同源物的酿酒酵母基因 RAD30 的缺失赋予了紫外线辐射敏感性和改变的突变性。
DOI：
10.1007/s004380050698
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Siede,W
中科院分区：
文献类型：
--
作者：
Roush,AA;Suarez,M;Friedberg,EC;Radman,M;Siede,W
ThedinBgene ofEscherichia coliis an SOS-inducible gene of unknown function. Its mode of regulation and the amino acid sequence similarity of the predicted DinB protein to the UmuC protein ofE. coliboth suggest a role in cellular responses to DNA damage and probably in error-prone repair. Proteins with sequence similarity to DinB have been predicted from genes cloned from various prokaryotic and eukaryotic organisms, includingCaenorhabditis elegans. Here we present the phenotypic characterization of a haploidSaccharomyces cerevisiaestrain deleted for the ORF YDR419W, encoding a yeast DinB homolog. The deletion mutant is viable but is moderately sensitive to killing following exposure to ultraviolet (UV) radiation. Hence, we have named the geneRAD30. Steady-state levels ofRAD30transcripts are increased following UV irradiation. UV-induced locus-specific reversion of anochreallele (arg4-17)is reduced in therad30deletion mutant. However, enhanced mutability was observed following treatment with the alkylating agent methylmethanesulfonate (MMS). Spontaneous mutability was also slightly increased. We conclude thatRAD30encodes an accessory function involved in DNA repair and mutagenesis. We speculate that the relatively weak phenotype and the opposite effects on mutability as a function of the type of DNA damage involved may derive from a functional redundancy of yeast proteins which facilitate replicative bypass of non-coding DNA lesions.
