The roles of different excision-repair mechanisms in the resistance of Micrococcus luteus to UV and chemical mutagens.
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 from 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, like recA- mutants of E. coli.
D015112:4-Nitroquinoline-1-oxide / Q000494:pharmacology; D004260:DNA Repair; D004706:Endodeoxyribonucleases; D008837:Micrococcus / Q000187:drug effects / Q000235:genetics* / Q000528:radiation effects; D009097:Multienzyme Complexes / Q000378:metabolism; D009153:Mutagens; D009699:N-Glycosyl Hydrolases; D011740:Pyrimidine Dimers / Q000378:metabolism; D014466:Ultraviolet Rays; D014965:X-Rays
D009097:Multienzyme Complexes; D009153:Mutagens; D011740:Pyrimidine Dimers; D015112:4-Nitroquinoline-1-oxide; C032219:UV endonuclease; D004706:Endodeoxyribonucleases; D009699:N-Glycosyl Hydrolases