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Analysis of the ciprofloxacin‐induced mutations in Salmonella typhimurium
Author(s) -
Clerch Berta,
Bravo Juan Manuel,
Llagostera Montserrat
Publication year - 1996
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/(sici)1098-2280(1996)27:2<110::aid-em6>3.0.co;2-k
Subject(s) - genetics , frameshift mutation , dna gyrase , biology , mutagen , plasmid , base pair , mutant , mutagenesis , mutation , salmonella , dna , gene , escherichia coli , microbiology and biotechnology , bacteria
The mutagenic events induced by ciprofloxacin, a potent antimicrobial agent, have been characterized. For this, a battery of His − mutants of Salmonella typhimurium ( hisG428 , hisG46 , hisC9070 , and hisG1775 targets) that detects the six possible transitions and transversions [Levin and Ames (1986): Environ Mutagen 8:9–28] and two additional His − strains ( hisC3076 and hisD3052 targets) carrying frameshift mutations have been used. Our results indicate that GC→TA transversions are the major base‐pair substitution induced by ciprofloxacin and that GC→AT transitions are also produced, but to a lesser degree. However, we cannot discard the fact that AT→TA transversions are also induced. In addition, the data indicate that the mutational specificity of ciprofloxacin depends on the location of the target. Intragenic base‐pair substitutions are the most frequent mutations at the hisG428 target when it is on the chromosome, whereas 3 or 6 base‐pair deletions are the major mutagenic events when this target is on the plasmid pAQ1. We have shown that ciprofloxacin also induces deletions/insertions at the hisC3076 and hisD3052 frameshift targets. Therefore, this inhibitor of DNA gyrase promotes a wide pattern of mutations including different kinds of base‐pair substitutions, 3 or 6 base‐pair deletions, and insertions/deletions resulting in frameshifts. All of these mutagenic events require the MucAB proteins involved in the error‐prone repair, with the exception of base‐pair insertions/deletions at the hisD3052 target, which are independent of the presence of plasmid pKM101. © 1996 Wiley‐Liss, Inc.

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