ACID SHOCK INDUCTION OF RPOS IS MEDIATED BY THE MOUSE VIRULENCE GENE MVIA OF SALMONELLA-TYPHIMURIUM

Citation
Smd. Bearson et al., ACID SHOCK INDUCTION OF RPOS IS MEDIATED BY THE MOUSE VIRULENCE GENE MVIA OF SALMONELLA-TYPHIMURIUM, Journal of bacteriology, 178(9), 1996, pp. 2572-2579
Citations number
59
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Microbiology
Journal title
ISSN journal
0021-9193
Volume
178
Issue
9
Year of publication
1996
Pages
2572 - 2579
Database
ISI
SICI code
0021-9193(1996)178:9<2572:ASIORI>2.0.ZU;2-R
Abstract
Salmonella typhimurium encounters a variety of acid stress situations during growth in host and nonhost environments, The organism can survi ve potentially lethal acid conditions (pH <4) if it is first able to a dapt to mild or more moderate acid levels. The molecular events that o ccur during this adaptive process are collectively referred to as the acid tolerance response and vary depending on whether the cells are in log- or stationary-phase growth. The acid tolerance response of logar ithmically growing cells includes the participation of an alternate si gma factor, sigma(S) (RpoS), commonly associated with stationary-phase physiology. Of 51 acid shock proteins (ASPs) induced during shifts to pH 4.4, 8 are clearly dependent on sigma(S) for production (I. S. Lee , J. Lin, H. K. Hall, B. Bearson, and J. W. Foster, Mol. Microbiol. 17 :155-167, 1995). The acid shock induction of these proteins appears to be the result of an acid shock-induced increase in the level of sigma (S) itself. We have discovered that one component of a potential signa l transduction system responsible for inducing rpoS expression is the product of the mouse virulence gene mviA(+). MviA exhibits extensive h omology to the regulatory components of certain two-component signal t ransduction systems (W. H. Benjamin, Jr., and P. D. Hall, abstr. B-67, p. 38, in Abstracts of the 93rd General Meeting of the American Socie ty for Microbiology 1993, 1993), Mutations in mviA (mviA::Km) caused t he overproduction of sigma(S) and sigma(S)-dependent ASPs in logarithm ically growing cells, as well as increases in tolerances to acid, heat , osmolarity, and oxidative stresses and significant decreases in grow th rate and colony size. Mutations in rpoS suppressed the mviA::Km-ass ociated defects in growth rate, colony size, ASP production, and stres s tolerance, suggesting that the effects of MviA on cell physiology oc cur via its control of sigma(S) levels. Western blot (immunoblot) anal yses of sigma(S) produced from natural or arabinose-regulated promoter s revealed that acid shock and MviA posttranscriptionally regulate sig ma(S) levels. Turnover experiments suggest that MviA regulates the sta bility of sigma(S) protein rather than the translation of rpoS message . We propose a model in which MviA or its unknown signal transduction partner senses some consequence of acid shock, and probably other stre sses, and signals the release of sigma(S) from proteolysis. The increa sed concentration of sigma(S) drives the elevated expression of the si gma(S)-dependent ASPs, resulting in an increase in stress tolerance, T he avirulent nature of mviA insertion mutants, therefore, appears to r esult from inappropriate sigma(S)-dependent gene expression during pat hogenesis.