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Regulatory RNAs and the HptB/RetS signalling pathways fine‐tune Pseudomonas aeruginosa pathogenesis
Author(s) -
Bordi Christophe,
Lamy MarieCécile,
Ventre Isabelle,
Termine Elise,
Hachani Abderrahman,
Fillet Sandy,
Roche Béatrice,
Bleves Sophie,
Méjean Vincent,
Lazdunski Andrée,
Filloux Alain
Publication year - 2010
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2010.07146.x
Subject(s) - biology , pseudomonas aeruginosa , regulator , quorum sensing , biofilm , regulation of gene expression , gene , microrna , gene expression , genetics , microbiology and biotechnology , response regulator , type three secretion system , virulence , bacteria , mutant
Summary Bacterial pathogenesis often depends on regulatory networks, two‐component systems and small RNAs (sRNAs). In Pseudomonas aeruginosa , the RetS sensor pathway downregulates expression of two sRNAs, rsmY and rsmZ . Consequently, biofilm and the Type Six Secretion System (T6SS) are repressed, whereas the Type III Secretion System (T3SS) is activated. We show that the HptB signalling pathway controls biofilm and T3SS, and fine‐tunes P. aeruginosa pathogenesis. We demonstrate that RetS and HptB intersect at the GacA response regulator, which directly controls sRNAs production. Importantly, RetS controls both sRNAs, whereas HptB exclusively regulates rsmY expression. We reveal that HptB signalling is a complex regulatory cascade. This cascade involves a response regulator, with an output domain belonging to the phosphatase 2C family, and likely an anti‐anti‐σ factor. This reveals that the initial input in the Gac system comes from several signalling pathways, and the final output is adjusted by a differential control on rsmY and rsmZ . This is exemplified by the RetS‐dependent but HptB‐independent control on T6SS. We also demonstrate a redundant action of the two sRNAs on T3SS gene expression, while the impact on pel gene expression is additive. These features underpin a novel mechanism in the fine‐tuned regulation of gene expression.