Mutation of luxS affects growth and virulence factor expression in Streptococcus pyogenes

Lyon, WR Madden, JC Levin, JC Stein, JL Caparon, MG

Wr. Lyon et al., Mutation of luxS affects growth and virulence factor expression in Streptococcus pyogenes, MOL MICROB, 42(1), 2001, pp. 145-157

61

INGLESE

Article

Microbiology

MOLECULAR MICROBIOLOGY

0950-382X → ACNP

42

1

2001

145 - 157

ISI

0950-382X(200110)42:1<145:MOLAGA>2.0.ZU;2-6

Adaptive responses of bacteria that involve sensing the presence of other b acteria are often critical for proliferation and the expression of virulenc e characteristics. The autoinducer II (AI-2) pathway has recently been show n to be a mechanism for sensing other bacteria that is highly conserved amo ng diverse bacterial species, including Gram-positive pathogens. However, a role for this pathway in the regulation of virulence factors in Gram-posit ive pathogens has yet to be established. In this study, we have inactivated luxS, an essential component of the AI-2 pathway, in the Gram-positive pat hogen Streptococcus pyogenes. Analyses of the resulting mutants revealed th e aberrant expression of several virulence properties that are regulated in response to growth phase, including enhanced haemolytic activity, and a dr amatic reduction in the expression of secreted proteolytic activity. This l atter defect was associated with a reduced ability to secrete and process t he precursor of the cysteine protease (SpeB) as well as a difference in the timing of expression of the protease. Enhanced haemolytic activity of the luxS strain was also shown to be linked with an increased expression of the haemolysin S-associated gene sagA. Disruptions of luxS in these mutants al so produced a media-dependent growth defect. Finally, an allelic replacemen t analysis of an S. pyogenes strain with a naturally occurring insertion of IS 1239 in luxS suggested a mechanism for modulation of virulence during i nfection. Results from this study suggest that luxS makes an important cont ribution to the regulation of S. pyogenes virulence factors.