Affiliation:
1. Department of Microbiology and Public Health, Michigan State University, East Lansing, Michigan, 48823
Abstract
The anti-tumor drug
cis
-platinum(II)diamminodichloride (PDD) induced extensive filamentation in wild-type
Escherichia coli
and in mutants lacking certain deoxyribonucleic acid (DNA) repair functions (
uvrA, recB, recC
, and
polA
); viability of repair-deficient mutants treated with PDD was significantly less than that of wild-type cells. PDD was highly toxic to
lex1, lex1 uvrA6
(where its effect was cummulative), and
recA13
mutants, all of which were killed without formation of filaments.
3
H-thymine incorporated into DNA of cells subsequently treated with PDD became trichloroacetic acid-soluble at rates similar to those observed after exposure to comparable doses of ultraviolet light (UV) or mitomycin C. PDD, like UV, induced extensive degradation of DNA in
recA
organisms. After a 30-min lag, PDD inhibited significantly the synthesis of DNA but not of ribonucleic acid or protein in
E. coli
. However, the relative differences between rates of DNA synthesis observed in PDD-treated and control cells decreased substantially when the duration of pulses (
3
H-thymine) was prolonged from 2 to 5 min. These observations suggest that PDD-induced damage to DNA is reversible, possibly by defined mechanisms of excision and recombination repair.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
132 articles.
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