US EPA

1022518 

Journal Article 

NaCl-sensitive mutant of Staphylococcus aureus has a Tn917-lacZ insertion in its ars operon 

Scybert, S; Pechous, R; Sitthisak, S; Nadakavukaren, MJ; Wilkinson, BJ; Jayaswal, RK 

2003 

Yes 

FEMS Microbiology Letters
ISSN: 0378-1097
EISSN: 1574-6968 

222 

2 

171-176 

English 

12770703 

10.1016/s0378-1097(03)00312-4 

WOS:000183239100003 

Staphylococcus aureus is a Gram-positive bacterium that is extremely halotolerant. To investigate the molecular mechanisms by which S. aureus can cope with osmotic stress, Tn917-lacZ-induced NaCl-sensitive mutants were isolated. An NaCl-sensitive mutant showed a longer lag period, slower growth rate, and lower final culture turbidity than the parent strain in liquid medium containing 1.5 M NaCl. Electron microscopic observation of the NaCl-sensitive mutant under NaCl stress conditions revealed large, pseudo-multicellular cells. Addition of exogenous osmoprotectants, such as glycine betaine, choline, L-proline, and proline betaine, did not relieve the NaCl sensitivity of the mutant. The region flanking the transposon insertion site in the NaCl-sensitive S. aureus chromosome was sequenced. The mutated gene was 99% identical to arsR, the arsenic operon regulatory protein present on the pI258 plasmid of S. aureus. The ars operon from pI258 was subcloned into the shuttle vector pLI50 and transferred into the NaCl-sensitive mutant. The ars operon in trans restored NaCl tolerance in the mutant, suggesting that NaCl sensitivity is due to the mutation in arsR. 

arsenic operon; osmoregulation; NaCl-sensitive mutant; Staphylococcus aureus