Differential regulation of the hmsCDE operon in Yersinia pestis and Yersinia pseudotuberculosis by the Rcs phosphorelay system.

Xiao-Peng Guo,Gai-Xian Ren,Yi-Cheng Sun,Xu-Jian Mao,Hui Zhu

doi:10.1038/srep08412

Xiao-Peng Guo, Gai-Xian Ren + Show 3 more

Open Access

https://doi.org/10.1038/srep08412

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Abstract

Yersinia pestis, the agent of plague, forms a biofilm in its flea vector to enhance transmission. Y. pestis biofilm development is positively regulated by hmsT and hmsD, encoding diguanylate cyclases (DGCs) involved in synthesis of the bacterial second messenger c-di-GMP. rcsA, encoding an auxiliary protein in Rcs phosphorelay, is nonfunctional in Y. pestis, while in Yersinia pseudotuberculosis, rcsA is functional and represses biofilms. Previously we showed that Rcs phosphorelay negatively regulates transcription of hmsT in Y. pestis and its ancestor Yersinia pseudotuberculosis. In this study, we show that Rcs positively regulates hmsCDE operon (encoding HmsD) in Y. pestis; while in the presence of functional rcsA, Rcs represses hmsCDE operon in Y. pseudotuberculosis. Loss of rcsA's function in Y. pestis not only causes derepression of hmsT but also causes activation of hmsD, which may account for the increased biofilm formation in Y. pestis. In addition, differential regulation of the two DGCs, HmsT and HmsD by Rcs may help Y. pestis to adapt to different environment.

Highlights

Differential regulation of the hmsCDE operon in Yersinia pestis and Yersinia pseudotuberculosis by the Rcs phosphorelay system
Y. pestis biofilm development is positively regulated by hmsT and hmsD, encoding diguanylate cyclases (DGCs) involved in synthesis of the bacterial second messenger c-di-GMP. rcsA, encoding an auxiliary protein in Rcs phosphorelay, is nonfunctional in Y. pestis, while in Yersinia pseudotuberculosis, rcsA is functional and represses biofilms
Loss of rcsA’s function in Y. pestis causes derepression of hmsT and causes activation of hmsD, which may account for the increased biofilm formation in Y. pestis

Summary

Introduction

Differential regulation of the hmsCDE operon in Yersinia pestis and Yersinia pseudotuberculosis by the Rcs phosphorelay system. The agent of plague, forms a biofilm in its flea vector to enhance transmission. Y. pestis biofilm development is positively regulated by hmsT and hmsD, encoding diguanylate cyclases (DGCs) involved in synthesis of the bacterial second messenger c-di-GMP. RcsA, encoding an auxiliary protein in Rcs phosphorelay, is nonfunctional in Y. pestis, while in Yersinia pseudotuberculosis, rcsA is functional and represses biofilms. We showed that Rcs phosphorelay negatively regulates transcription of hmsT in Y. pestis and its ancestor Yersinia pseudotuberculosis. Differential regulation of the two DGCs, HmsT and HmsD by Rcs may help Y. pestis to adapt to different environment. The Y. pestis genome encodes two DGCs, HmsT and HmsD, related to biofilm formation[7,8,9,10]. HmsT plays a major role on in vitro biofilm formation, while HmsD plays a more prominent role in producing proventricular-blocking biofilm in the flea[10]

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