Radiosensitive and mitotic recombination phenotypes of the Saccharomyces cerevisiae dun1 mutant defective in DNA damage-inducible gene expression.
Radiosensitive and mitotic recombination phenotypes of the Saccharomyces cerevisiae dun1 mutant defective in DNA damage-inducible gene expression.
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DNA 损伤诱导基因表达缺陷的酿酒酵母 dun1 突变体的放射敏感性和有丝分裂重组表型。
DOI：
10.1093/genetics/152.3.909
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发表时间：
1999
期刊：
影响因子：
3.3
通讯作者：
Cera,C
中科院分区：
文献类型：
--
作者：
Fasullo,M;Koudelik,J;AhChing,P;Giallanza,P;Cera,C
DNA损伤诱导的基因表达在增强对DNA损伤剂的抗性方面的生物学意义尚不清楚。我们研究了DUN1介导的、DNA损伤诱导的基因表达在酿酒酵母抗辐射能力中的作用。通过对dun1、rad52、rad1、rad9、rad18单突变体和双突变体以及dun1 rad9 rad52三突变体的辐射敏感性测定，将DUN1基因归入Rad3上位性群。在紫外线敏感性方面，dun1和rad52单突变体相似，而dun1 rad52双突变体则表现出协同降低的抗紫外线能力。与DUN1株相比，Dun1突变体中两个ade2等位基因之间自发的染色体内和异等位基因转换事件均增加，并且这种增强的重组依赖于RAD52而不是Rad1基因功能。在dun1突变体中，截短的his3片段之间的自发姐妹染色单体交换(SCE)没有增强，但UV诱导的姐妹染色单体交换和异型等位基因重组增强。电离辐射和甲磺酸甲酯(MMS)诱导的DNA损伤在Dun1突变株中没有表现出比DUN1株更大的重组原性。我们认为，DUN1介导的DNA损伤诱导基因表达的一个功能是将紫外线损伤的修复引导到非重组修复途径。
The biological significance of DNA damage-induced gene expression in conferring resistance to DNA-damaging agents is unclear. We investigated the role of DUN1-mediated, DNA damage-inducible gene expression in conferring radiation resistance in Saccharomyces cerevisiae. The DUN1 gene was assigned to the RAD3 epistasis group by quantitating the radiation sensitivities of dun1, rad52, rad1, rad9, rad18 single and double mutants, and of the dun1 rad9 rad52 triple mutant. The dun1 and rad52 single mutants were similar in terms of UV sensitivities; however, the dun1 rad52 double mutant exhibited a synergistic decrease in UV resistance. Both spontaneous intrachromosomal and heteroallelic gene conversion events between two ade2 alleles were enhanced in dun1 mutants, compared to DUN1 strains, and elevated recombination was dependent on RAD52 but not RAD1 gene function. Spontaneous sister chromatid exchange (SCE), as monitored between truncated his3 fragments, was not enhanced in dun1 mutants, but UV-induced SCE and heteroallelic recombination were enhanced. Ionizing radiation and methyl methanesulfonate (MMS)-induced DNA damage did not exhibit greater recombinogenicity in the dun1 mutant compared to the DUN1 strain. We suggest that one function of DUN1-mediated DNA damage-induced gene expression is to channel the repair of UV damage into a nonrecombinogenic repair pathway.