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HmsC , a periplasmic protein, controls biofilm formation via repression of HmsD , a diguanylate cyclase in Y ersinia pestis
Author(s) -
Ren GaiXian,
Yan HaiQin,
Zhu Hui,
Guo XiaoPeng,
Sun YiCheng
Publication year - 2014
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.12323
Subject(s) - biofilm , periplasmic space , biology , microbiology and biotechnology , yersinia pestis , operon , virulence , gene , biochemistry , bacteria , genetics , mutant , escherichia coli
Summary Y ersinia pestis , the cause of plague, forms a biofilm in the foregut of its flea vector to enhance transmission. Biofilm formation in Y . pestis is controlled by the intracellular levels of the second messenger molecule cyclic diguanylate ( c ‐ di ‐ GMP ). HmsT and Y 3730, the two diguanylate cyclases (DGC) in Y . pestis , are responsible for the synthesis of c ‐ di ‐ GMP . Y 3730, which we name here as HmsD , has little effect on in vitro biofilms, but has a major effect on biofilm formation in the flea. The mechanism by which HmsD plays differential roles in vivo and in vitro is not understood. In this study, we show that hmsD is part of a three‐gene operon ( y 3729‐31), which we designate as hmsCDE . Deletion of hmsC resulted in increased, hmsD ‐dependent biofilm formation, while deletion or overexpression of hmsE did not affect biofilm formation. Localization experiments suggest that HmsC resides in the periplasmic space. In addition, we provide evidence that HmsC might interact directly with the periplasmic domain of HmsD and cause the proteolysis of HmsD . We propose that HmsC senses the environmental signals, which in turn regulates HmsD , and controls the c ‐ di ‐ GMP synthesis and biofilm formation in Y . pestis .