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

用MNNG处理亲本ATCC4698菌株后，分离出对UV和4-NQO均敏感的黄体分枝杆菌突变体。突变体对丝裂霉素C、顺铂、8-甲氧基补骨脂素(8-MOP) +近紫外线和当归素+近紫外线也有不同程度的高度敏感。紫外辐照DNA中嘧啶二聚体的内切酶活性通常在突变体的提取物中检测到。在宿主细胞再激活能力方面，突变体可分为两组。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射线有抵抗力。在用当归黄芪加近紫外线处理后，hcr^-突变体在孵育期间没有发生DNA的切割，而在亲本菌株中发生了DNA的切割。事实表明，hcr突变体在切口机制上存在缺陷，具有广泛的底物特异性，类似于大肠杆菌的UVRABC核酸酶。另一方面，在hcr^-突变体和亲本菌株中，DNA的切割和紫外线诱导的胸腺嘧啶二聚体的去除都发生在DNA中，这归因于紫外线内切酶活性。与hcr^-突变体相比，hcr^+突变体对x射线高度敏感，没有像大肠杆菌的recA^-突变体那样引起紫外光引起的红霉素耐药突变。

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.