Molecular mechanism of pyrimidine dimer excision in Saccharomyces cerevisiae. I. Studies with intact cells and cell-free systems.
Molecular mechanism of pyrimidine dimer excision in Saccharomyces cerevisiae. I. Studies with intact cells and cell-free systems.
复制标题
酿酒酵母嘧啶二聚体切除的分子机制。
DOI：
10.1007/978-1-4684-3842-0_8
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
Friedberg,EC
中科院分区：
文献类型：
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作者：
Reynolds,RJ;Friedberg,EC
我们已经调查了从野生型和紫外线敏感突变体的酵母Saccharomycescerevisiae的DNA中切除嘧啶二聚体的一些方面。我们的研究表明，RAD 3组中的许多突变体（rad 1 -2，rad 1 -11; rad 2 -2，rad 2 -4; rad 3 - 1; rad 4 - 2，rad 4 - 3）在体内嘧啶二聚体切除方面相对于野生型菌株是有缺陷的，在UV孵育后其DNA单链断裂的产生也是有缺陷的。紫外线诱导的孵育独立的单链断裂的存在下，防止明确的结论有关的作用，各种RAD基因座在切口过程中，但提供了证据的生化细分的RAD 3组基因座。使用紫外线照射的DNA preincised与二聚体特异性核酸内切酶活性从藤黄微球菌，我们也检测到酶活性从野生型酵母提取物催化的选择性切除的胸腺嘧啶二聚体。在迄今为止检测的所有突变株中（rad 1 -11; rad 2 -4; rad 3 - 1; rad 4 - 3），这种活性都处于正常水平。因此，在酵母菌中，9个控制嘧啶二聚体切除的基因座中，至少有4个影响与DNA切割或预切割相关的事件。这种情况与在人类疾病着色性干皮病中观察到的许多互补组惊人地相似。
We have investigated a number of aspects of the excision of pyrimidine dimers from the DNA of wild-type and UV sensitive mutants of the yeastSaccharomyces cerevisiae. Our studies show that a number ofradmutants in the RAD3 group (rad1-2,rad1-11;rad2-2,rad2-4;rad3−l;rad4−2,rad4−3) that are defective relative to wild-type strains in pyrimidine dimer excision in vivo, are also defective in the production of single strand breaks in their DNA during post-UV incubation. The presence of UV-induced incubation-independent single-strand breaks prevents definitive conclusions regarding the role of various RAD loci in the incision process but provides evidence of a biochemical subdivision in the RAD3 group loci. Using UV irradiated DNA preincised with dimer-specific endonuclease activity fromMicrococcus luteus, we have also detected enzymatic activity from extracts of wild-type yeast that catalyzes the selective excision of thymine-containing pyrmidine dimers. Normal levels of this activity are present in all mutant strains thus far examined (rad1-11;rad2-4;rad3−l;rad4−3).Thus, inSaccharomyces cerevisiaeit appears that at least four of the nine genetic loci governing pyrimidine dimer excision affect events associated with DNA incision or preincision. This situation is strikingly analagous to that observed with the numerous complementation groups in the human disease xeroderma pigmentosum.