1987 Fiscal Year Final Research Report Summary
The roles of diferent DNA repair mechanisms in the resistance of Micrococcus luteus to UV and chemical mutagens
| Project/Area Number |
61580178
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
放射線5生物学
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| Research Institution | Kyoto University |
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Principal Investigator |
YONEI Shuji Faculty of Science, Kyoto University, 理学部, 講師 (60093340)
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| Project Period (FY) |
1986 – 1987
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| Keywords | Micococcus luteus / DNA repair / UV endonuclease / UV / psoralens / chemical mutagens / UV-sensitive mutants / ピリミジンダイマー |
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| Research Abstract |
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.
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