The roles of diferent DNA repair mechanisms in the resistance of Micrococcus luteus to UV and chemical mutagens

不同DNA修复机制在藤黄微球菌抵抗紫外线和化学诱变剂中的作用

• 批准号: 61580178
• 负责人: YONEI Shuji
• 金额: $ 1.34万
• 依托单位: Kyoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1986
• 资助国家: 日本
• 起止时间: 1986 至 1987
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-61580178/
• 关键词: Micococcus luteus; DNA repair; UV endonuclease; UV; psoralens; chemical mutagens; UV-sensitive mutants; ピリミジンダイマー; Micrococcus luteus; UVエンドヌクレアーゼ; DNA損傷

M. luteus mutants showing increased sensitivity to both UV and 4-NQO were isolated after the treatment of parental ATCC4698 strain with MNNG. The mutants were also highly sensitive to mitomycin C, cis-platinum, 8-methoxypsoralen (8-MOP) plus near-UV and angelicin plus near-UV in various degrees. The endonuclease activity specific for pyrimidine dimers in UV-irradiated DNA was normally detected in extract of the mutants. With regard to host-cell reactivation ability the mutants fell into two groups. The hcr^- mutants lacked the ability to reactivate UV-damaged N6 phage and were resistant to X-rays. The incision of DNA did not occur during incubation after the treatment with angelicin plus near-UV in the hcr^- mutants, whereas it occurred in the parental strain. The facts indicate that the hcr mutants are defective in the incision mechanism which has a wide substrate specificity, similar to the UVRABC nuclease of E. coli. On the other hand, the incision of DNA and the removal of UV-induced thymine dimers form DNA occurred in the hcr^- mutants as well as in the parental strain, which is ascribed to the UV endonuclease activity. Compared with the hcr^- mutants, hcr^+ mutants were highly sensitive to X-rays and showed no induction of erythromycin-resistant mutation due to UV, like recA^- mutants of E. coli.

M.在用MNNG处理亲本ATCC 4698菌株后，分离出对UV和4-NQO敏感性增加的黄体突变体。突变株对丝裂霉素C、顺铂、8-甲氧基芘（8-MOP）加近紫外线和当归素加近紫外线也有不同程度的敏感性。在突变体的提取物中通常检测到对UV照射的DNA中的嘧啶二聚体具有特异性的核酸内切酶活性。关于宿主细胞的再活化能力，突变体分为两组。hcr^-突变体缺乏重新激活紫外线损伤的N6噬菌体的能力，并且对X射线具有抗性。在用当归素加近紫外线处理后的培养过程中，hcr^-突变体的DNA没有发生切割，而在亲本菌株中发生了切割。这些事实表明，hcr突变体在切割机制上存在缺陷，具有广泛的底物特异性，类似于大肠杆菌UVRABC核酸酶。杆菌另一方面，在hcr^-突变体和亲本菌株中，DNA的切割和UV诱导的胸腺嘧啶二聚体从DNA中的去除都发生在hcr^-突变体中，这归因于UV内切酶活性。与hcr^-突变体相比，hcr^+突变体对X射线高度敏感，且不像大肠杆菌的recA^-突变体那样显示出由紫外线引起的红霉素抗性突变。杆菌

项目成果

Kazuyuki Tao;Asao Noda;Shuji Yonei: Mutation Res.(1987)

陶和之；野田麻生；米内修二：突变研究（1987）

Kazuyuki Tao;Shuji Yonei;Asao Noda: J.Radiat.Res.27. 25 (1985)

Kazuyuki Tao；Shuji Yonei；Asao Noda：J.Radiat.Res.27。

Kazuyuki Tao, Asao Noda and Shuji Yonei: "The roles of different excision-repair mechanisms in the resistance of Micococcus luteus to UV and chemical mutagens" Mutation Research. 183. 231-239 (1987)

Kazuyuki Tao、Asao Noda 和 Shuji Yonei：“不同切除修复机制在藤黄微球菌对紫外线和化学诱变剂的抵抗中的作用”突变研究。

Shuji Yonei and Kazuyuki Tao: "An endonucleolytic activity from Micrococcus luteus directed towards angelicin monoadducts in DNA"

Shuji Yonei 和 Kazuyuki Tai：“藤黄微球菌针对 DNA 中当归素单加合物的核酸内切活性”

Kazuyuki Tao;Asao Noda and Shuji Yonei: Mutation Research. 183. 231-239 (1987)

Kazuyuki Tao；Asao Noda 和 Shuji Yonei：突变研究。