Abstract
The processing of damaged DNA was altered in a mitomycin C-sensitive mutant
(mtcA) of Micrococcus radiodurans. Even though the mutant retained resistance
to 254-nm UV radiation, it did not, in contrast to the wild-type strain, show any
excessive DNA degradation or cell death when incubated with chloramphenicol
after sublethal doses of either UV light or mitomycin C. The results suggest the
constitutive synthesis of an enzyme system responsible for wild-type proficiency
in the repair of mitomycin C-induced damage. An alternative system able to repair
damage caused by mitomycin C was demonstrated in the mtcA background. In
this strain, additional damage infficted upon the cellular DNA effected a massive
rescue of cells previously inactivated by mitomycin C. Rescue was provoked by
ionizing radiation, by UV light, or by simple alkylating agents. Cells treated with
psoralen plus near-UV radiation could be rescued only when inactivation was due
primarily to psoralen-DNA interstrand cross-links rather than to monoadducts.
The rescue of inactivated cells.was prevented in the presence of chloramphenicol.
These results can be interpreted most readily in terms of an alternative repair
system able to overcome DNA interstrand cross-links produced by mitomycin C
or psoralen plus near-UV light, but induced only by the more abundant number of
damages produced by radiation or simple alkylating agents.
Original language | English |
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Journal | Journal of Bacteriology |
Volume | 152 |
Issue number | 3 |
Pages (from-to) | 976-982 |
ISSN | 0021-9193 |
Publication status | Published - 1982 |