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首页> 外文期刊>Genes & Genetic Systems >Genetic analysis of the Neurospora crassa RAD14 homolog mus-43 and the RAD10 homolog mus-44 reveals that they belong to the mus-38 pathway of two nucleotide excision repair systems.
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Genetic analysis of the Neurospora crassa RAD14 homolog mus-43 and the RAD10 homolog mus-44 reveals that they belong to the mus-38 pathway of two nucleotide excision repair systems.

机译：对芥菜神经孢菌RAD14同源mus-43和RAD10同源mus-44的遗传分析表明，它们属于两个核苷酸切除修复系统的mus-38途径。

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摘要

Saccharomyces cerevisiae Rad14 and Rad10 proteins are essential for nucleotide excision repair (NER). Rad14 is a UV-damaged DNA binding protein and Rad10 is a structure-specific endonuclease that functions in a complex with Rad1. In this study, we identified and characterized the RAD14 and RAD10 homolog genes in Neurospora crassa, which we named mus-43 and mus-44, respectively. Disruption of mus-43 and mus-44 conferred sensitivity to UV and 4-nitroquinoline 1-oxide, but not to methyl methanesulfonate, N-methyl-N'-nitro-N-nitrosoguanidine, camptothecin, hydroxyurea, or bleomycin. The mus-44 mutant was more sensitive to UV than the mus-43 mutant. Genetic analysis indicated that mus-43 and mus-44 are epistatic to mus-38 which is a homolog of the S. cerevisiae RAD1, but not to mus-18 which belongs to a second excision repair pathway. Immunological assays demonstrated that both mus-43 and mus-44 retained the ability to excise UV-induced cyclobutane pyrimidine dimers and 6-4 photoproducts, but that excision ability was completely abolished in the mus-43 mus-18 and mus-44 mus-18 double mutants. These double mutants exhibited extremely high sensitivity to UV. In mus-43 and mus-44 mutants, the UV-induced mutation frequency increased compared to that of the wild-type. The mus-44 mutants also exhibited a partial photoreactivation defect phenotype similar to mus-38. These results suggest that both mus-43 and mus-44 function in the mus-38 NER pathway, but not in the mus-18 excision repair pathway.
机译：酿酒酵母Rad14和Rad10蛋白对于核苷酸切除修复（NER）是必不可少的。 Rad14是紫外线损伤的DNA结合蛋白，Rad10是结构特异性核酸内切酶，可与Rad1形成复合体。在这项研究中，我们鉴定和表征了神经孢菌中的RAD14和RAD10同源基因，我们分别命名为mus-43和mus-44。破坏mus-43和mus-44赋予了对UV和4-硝基喹啉1氧化物的敏感性，但对甲磺酸甲酯，N-甲基-N'-硝基-N-亚硝基胍，喜树碱，羟基脲或博来霉素不敏感。 mus-44突变体比mus-43突变体对紫外线更敏感。遗传分析表明，mus-43和mus-44对mus-38（它是酿酒酵母RAD1的同系物）具有上位性，但对mus-18（属于第二条切除修复途径）不具有上位性。免疫学分析表明，mus-43和mus-44都保留了切除紫外线诱导的环丁烷嘧啶二聚体和6-4 photoproducts的能力，但mus-43 mus-18和mus-44 mus- 18个双突变体。这些双重突变体对紫外线表现出极高的敏感性。与野生型相比，在mus-43和mus-44突变体中，紫外线诱导的突变频率增加。 mus-44突变体还表现出类似于mus-38的部分光活化缺陷表型。这些结果表明，mus-43和mus-44在mus-38 NER途径中均起作用，但在mus-18切除修复途径中均不起作用。

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