BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia

Abstract c-di-GMP is a cellular second messenger that regulates diverse bacterial processes, including swimming, biofilm formation and virulence. However, in Stenotrophomonas maltophilia, a nosocomial pathogen that frequently infects immunodeficient or immunoincompetent patients, the regulatory func...

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Autores principales: Wei Liu, Xiu-Qi Tian, Jin-Wei Wei, Li-Li Ding, Wei Qian, Zhong Liu, Fang-Fang Wang
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/c51dec385fef452fac55864f89617ce9
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spelling oai:doaj.org-article:c51dec385fef452fac55864f89617ce92021-12-02T11:52:31ZBsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia10.1038/s41598-017-04763-w2045-2322https://doaj.org/article/c51dec385fef452fac55864f89617ce92017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04763-whttps://doaj.org/toc/2045-2322Abstract c-di-GMP is a cellular second messenger that regulates diverse bacterial processes, including swimming, biofilm formation and virulence. However, in Stenotrophomonas maltophilia, a nosocomial pathogen that frequently infects immunodeficient or immunoincompetent patients, the regulatory function of c-di-GMP remains unclear. Here we show that BsmR is a negative regulator of biofilm development that degrades c-di-GMP through its EAL domain. Increasing BsmR expression resulted in significant increase in bacterial swimming and decrease in cell aggregation. BsmR regulates the expression of at least 349 genes. Among them, 34 involved in flagellar assembly and a flagellar-assembly-related transcription factor (fsnR) are positively regulated. Although BsmR is a response regulator of the two-component signaling system, its role in biofilm formation depends on the expression level of its respective gene (bsmR), not on the protein’s phosphorylation level. A transcription factor, BsmT, whose coding gene is located in the same tetra-cistronic operon as bsmR, was shown to directly bind to the promoter region of the operon and, through a positive regulatory loop, modulate bsmR transcription. Thus, our results revealed that the c-di-GMP signaling pathway controls biofilm formation and swimming in S. maltophilia, suggesting c-di-GMP signaling as a target in the development of novel antibacterial agents to resist this pathogen.Wei LiuXiu-Qi TianJin-Wei WeiLi-Li DingWei QianZhong LiuFang-Fang WangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-15 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Wei Liu
Xiu-Qi Tian
Jin-Wei Wei
Li-Li Ding
Wei Qian
Zhong Liu
Fang-Fang Wang
BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia
description Abstract c-di-GMP is a cellular second messenger that regulates diverse bacterial processes, including swimming, biofilm formation and virulence. However, in Stenotrophomonas maltophilia, a nosocomial pathogen that frequently infects immunodeficient or immunoincompetent patients, the regulatory function of c-di-GMP remains unclear. Here we show that BsmR is a negative regulator of biofilm development that degrades c-di-GMP through its EAL domain. Increasing BsmR expression resulted in significant increase in bacterial swimming and decrease in cell aggregation. BsmR regulates the expression of at least 349 genes. Among them, 34 involved in flagellar assembly and a flagellar-assembly-related transcription factor (fsnR) are positively regulated. Although BsmR is a response regulator of the two-component signaling system, its role in biofilm formation depends on the expression level of its respective gene (bsmR), not on the protein’s phosphorylation level. A transcription factor, BsmT, whose coding gene is located in the same tetra-cistronic operon as bsmR, was shown to directly bind to the promoter region of the operon and, through a positive regulatory loop, modulate bsmR transcription. Thus, our results revealed that the c-di-GMP signaling pathway controls biofilm formation and swimming in S. maltophilia, suggesting c-di-GMP signaling as a target in the development of novel antibacterial agents to resist this pathogen.
format article
author Wei Liu
Xiu-Qi Tian
Jin-Wei Wei
Li-Li Ding
Wei Qian
Zhong Liu
Fang-Fang Wang
author_facet Wei Liu
Xiu-Qi Tian
Jin-Wei Wei
Li-Li Ding
Wei Qian
Zhong Liu
Fang-Fang Wang
author_sort Wei Liu
title BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia
title_short BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia
title_full BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia
title_fullStr BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia
title_full_unstemmed BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia
title_sort bsmr degrades c-di-gmp to modulate biofilm formation of nosocomial pathogen stenotrophomonas maltophilia
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/c51dec385fef452fac55864f89617ce9
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