A non-coding RNA promotes bacterial persistence and decreases virulence by regulating a regulator in Staphylococcus aureus.

Staphylococcus aureus produces a high number of RNAs for which the functions are poorly understood. Several non-coding RNAs carry a C-rich sequence suggesting that they regulate mRNAs at the post-transcriptional level. We demonstrate that the Sigma B-dependent RsaA RNA represses the synthesis of the...

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Autores principales: Cédric Romilly, Claire Lays, Arnaud Tomasini, Isabelle Caldelari, Yvonne Benito, Philippe Hammann, Thomas Geissmann, Sandrine Boisset, Pascale Romby, François Vandenesch
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Acceso en línea:https://doaj.org/article/d2ed90c785b14249bc496eaf4bbcf1c2
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spelling oai:doaj.org-article:d2ed90c785b14249bc496eaf4bbcf1c22021-11-18T06:06:49ZA non-coding RNA promotes bacterial persistence and decreases virulence by regulating a regulator in Staphylococcus aureus.1553-73661553-737410.1371/journal.ppat.1003979https://doaj.org/article/d2ed90c785b14249bc496eaf4bbcf1c22014-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24651379/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Staphylococcus aureus produces a high number of RNAs for which the functions are poorly understood. Several non-coding RNAs carry a C-rich sequence suggesting that they regulate mRNAs at the post-transcriptional level. We demonstrate that the Sigma B-dependent RsaA RNA represses the synthesis of the global transcriptional regulator MgrA by forming an imperfect duplex with the Shine and Dalgarno sequence and a loop-loop interaction within the coding region of the target mRNA. These two recognition sites are required for translation repression. Consequently, RsaA causes enhanced production of biofilm and a decreased synthesis of capsule formation in several strain backgrounds. These phenotypes led to a decreased protection of S. aureus against opsonophagocytic killing by polymorphonuclear leukocytes compared to the mutant strains lacking RsaA. Mice animal models showed that RsaA attenuates the severity of acute systemic infections and enhances chronic catheter infection. RsaA takes part in a regulatory network that contributes to the complex interactions of S. aureus with the host immune system to moderate invasiveness and favour chronic infections. It is the first example of a conserved small RNA in S. aureus functioning as a virulence suppressor of acute infections. Because S. aureus is essentially a human commensal, we propose that RsaA has been positively selected through evolution to support commensalism and saprophytic interactions with the host.Cédric RomillyClaire LaysArnaud TomasiniIsabelle CaldelariYvonne BenitoPhilippe HammannThomas GeissmannSandrine BoissetPascale RombyFrançois VandeneschPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 10, Iss 3, p e1003979 (2014)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Cédric Romilly
Claire Lays
Arnaud Tomasini
Isabelle Caldelari
Yvonne Benito
Philippe Hammann
Thomas Geissmann
Sandrine Boisset
Pascale Romby
François Vandenesch
A non-coding RNA promotes bacterial persistence and decreases virulence by regulating a regulator in Staphylococcus aureus.
description Staphylococcus aureus produces a high number of RNAs for which the functions are poorly understood. Several non-coding RNAs carry a C-rich sequence suggesting that they regulate mRNAs at the post-transcriptional level. We demonstrate that the Sigma B-dependent RsaA RNA represses the synthesis of the global transcriptional regulator MgrA by forming an imperfect duplex with the Shine and Dalgarno sequence and a loop-loop interaction within the coding region of the target mRNA. These two recognition sites are required for translation repression. Consequently, RsaA causes enhanced production of biofilm and a decreased synthesis of capsule formation in several strain backgrounds. These phenotypes led to a decreased protection of S. aureus against opsonophagocytic killing by polymorphonuclear leukocytes compared to the mutant strains lacking RsaA. Mice animal models showed that RsaA attenuates the severity of acute systemic infections and enhances chronic catheter infection. RsaA takes part in a regulatory network that contributes to the complex interactions of S. aureus with the host immune system to moderate invasiveness and favour chronic infections. It is the first example of a conserved small RNA in S. aureus functioning as a virulence suppressor of acute infections. Because S. aureus is essentially a human commensal, we propose that RsaA has been positively selected through evolution to support commensalism and saprophytic interactions with the host.
format article
author Cédric Romilly
Claire Lays
Arnaud Tomasini
Isabelle Caldelari
Yvonne Benito
Philippe Hammann
Thomas Geissmann
Sandrine Boisset
Pascale Romby
François Vandenesch
author_facet Cédric Romilly
Claire Lays
Arnaud Tomasini
Isabelle Caldelari
Yvonne Benito
Philippe Hammann
Thomas Geissmann
Sandrine Boisset
Pascale Romby
François Vandenesch
author_sort Cédric Romilly
title A non-coding RNA promotes bacterial persistence and decreases virulence by regulating a regulator in Staphylococcus aureus.
title_short A non-coding RNA promotes bacterial persistence and decreases virulence by regulating a regulator in Staphylococcus aureus.
title_full A non-coding RNA promotes bacterial persistence and decreases virulence by regulating a regulator in Staphylococcus aureus.
title_fullStr A non-coding RNA promotes bacterial persistence and decreases virulence by regulating a regulator in Staphylococcus aureus.
title_full_unstemmed A non-coding RNA promotes bacterial persistence and decreases virulence by regulating a regulator in Staphylococcus aureus.
title_sort non-coding rna promotes bacterial persistence and decreases virulence by regulating a regulator in staphylococcus aureus.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/d2ed90c785b14249bc496eaf4bbcf1c2
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