Investigation of the Mutator Genes in Staphylococcus aureusN. Trong Hiep* and B. Tung Hiep
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In contrast to Escherichia coli, the mechanisms of hypermutability have been poorly studied in Staphylococcus aureus, only the role of mutSL has been recently demonstrated. The in silico analysis of the genome of S. aureus MW2 allowed to identify thirty-four homologues of genes reported as mutators in E. coli or Bacillus subtilis. Six candidate genes in S. aureus, homologues of miaA, nth, ung, recA, recG and mutS2, were chosen on the basis of their co-existence in E. coli, B. subtilis and S. aureus, and of a high percentage of similarity of the deduced amino acid sequences (36%, 21%, 54%, 59%, 35% and 26% identity between E. coli and S. aureus and 48%, 63%, 48%, 68%, 50%, and 50% identity between B. subtilis and S. aureus, respectively). Individual genes of S. aureus RN4220 were inactivated by insertion of the thermosensitive pBT1 plasmid. Only mutants of nth gene showed an increase in frequencies of mutation to rifampin (mean 1.6 x 10-7) and streptomycin resistance (mean 3.1 x 10-6), versus 1.9 x 10-8 and 5.1 x 10-7 in the parent strain, respectively. Complementation of the mutant by an intact nth gene allowed to restore the mutation frequency similar to that of the wild-type. To the best of our knowledge, nth gene may play a part at the hypermutability other than mutSL in S. aureus.
Keyword:
mutator gene, Staphylococcus aureus, Escherichia coli, Bacillus subtilis, mutation
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