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H fq‐dependent, co‐ordinate control of cyclic diguanylate synthesis and catabolism in the plague pathogen Y ersinia pestis
Author(s) -
Bellows Lauren E.,
Koestler Benjamin J.,
Karaba Sara M.,
Waters Christopher M.,
Lathem Wyndham W.
Publication year - 2012
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/mmi.12011
Subject(s) - biology , biofilm , messenger rna , microbiology and biotechnology , rna , pathogen , biochemistry , genetics , gene , bacteria
Summary Y ersinia pestis , the cause of the disease plague, forms biofilms to enhance flea‐to‐mammal transmission. Biofilm formation is dependent on exopolysaccharide synthesis and is controlled by the intracellular levels of the second messenger molecule cyclic diguanylate (c‐di‐ GMP ), but the mechanisms by which Y . pestis regulates c‐di‐ GMP synthesis and turnover are not fully understood. Here we show that the small RNA chaperone H fq contributes to the regulation of c‐di‐ GMP levels and biofilm formation by modulating the abundance of both the c‐di‐ GMP phosphodiesterase HmsP and the diguanylate cyclase HmsT . To do so, H fq co‐ordinately promotes hmsP m RNA accumulation while simultaneously decreasing the stability of the hmsT transcript. H fq‐dependent regulation of HmsP occurs at the transcriptional level while the regulation of HmsT is post‐transcriptional and is localized to the 5′ untranslated region/proximal coding sequence of the hmsT transcript. Decoupling HmsP from H fq‐based regulation is sufficient to overcome the effects of Δ hfq on c‐di‐ GMP and biofilm formation. We propose that Y . pestis utilizes H fq to link c‐di‐ GMP levels to environmental conditions and that the disregulation of c‐di‐ GMP turnover in the absence of H fq may contribute to the severe attenuation of Y . pestis lacking this RNA chaperone in animal models of plague.