Journal
MOLECULAR MICROBIOLOGY
Volume 89, Issue 5, Pages 989-1002Publisher
WILEY
DOI: 10.1111/mmi.12325
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Funding
- National Science Foundation [MCB-0919821]
- National Institutes of Health [5U19AI090872-03]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI090872] Funding Source: NIH RePORTER
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Biofilms promote attachment of Vibrio cholerae in aquatic ecosystems and aid in transmission. Intracellular c-di-GMP levels that control biofilm development positively correlate with expression of Qrr sRNAs, which are transcribed when quorum sensing (QS) autoinducer levels are low. The Qrr sRNAs base-pair with and repress translation of hapR encoding the QS master regulator', hence increased c-di-GMP and biofilm development at low density were believed to be solely a consequence of Qrr/hapR pairing. We show that Qrr sRNAs also base-pair with and activate translation of the mRNA of a diguanylate cyclase (DGC), Vca0939; relieving an inhibitory structure in vca0939 that occludes the ribosome binding site. A nucleotide substitution in vca0939 disrupted sRNA/mRNA base-pairing and prevented vca0939 translation, while a compensating Qrr sRNA substitution restored pairing and Vca0939 levels. Qrr-dependent DGC activation led to c-di-GMP accumulation and biofilm development in V.cholerae. This represents the first description of (1) a DGC post-transcriptionally activated by direct pairing with an Hfq-dependent sRNA, and (2) control of a V.choleraeQS phenotype, independent of HapR. Thus, direct interactions of the same sRNAs with two mRNAs promote c-di-GMP-dependent biofilm formation by complementary mechanisms in V.cholerae; by negatively regulating HapR, and positively regulating the DGC Vca0939.
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