HmsC, a periplasmic protein, controls biofilm formation via repression of HmsD, a diguanylate cyclase in Yersinia pestis
HmsC, a periplasmic protein, controls biofilm formation via repression of HmsD, a diguanylate cyclase in Yersinia pestis
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DOI：
10.1111/1462-2920.12323
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发表时间：
2014-04-01
影响因子：
5.1
通讯作者：
Sun, Yi-Cheng
中科院分区：
文献类型：
--
作者：
Ren, Gai-Xian;Yan, Hai-Qin;Sun, Yi-Cheng
鼠疫耶尔森氏菌是鼠疫的致病菌，它在跳蚤的前肠中形成生物膜以增强传播。在Y.鼠疫杆菌是由第二信使分子环二鸟苷酸（c-di-GMP）的细胞内水平控制的。HmsT和Y3730是Y.鼠疫杆菌负责合成c-di-GMP。Y3730，我们在此命名为HmsD，对体外生物膜几乎没有影响，但对跳蚤中的生物膜形成有主要影响。HmsD在体内和体外发挥不同作用的机制尚不清楚。在这项研究中，我们表明，hmsD是一个三基因操纵子（y3729-31），我们指定为hmsCDE的一部分。hmsC的缺失导致增加，hmsD依赖的生物膜形成，而hmsE的缺失或过表达不影响生物膜形成。定位实验表明，HmsC驻留在周质空间。此外，我们提供的证据表明，HmsC可能直接与HmsD的周质结构域，并导致HmsD的蛋白水解。我们认为HmsC感受环境信号，进而调节HmsD，并控制Y中c-di-GMP的合成和生物膜的形成。鼠疫
Yersinia 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 Y3730, the two diguanylate cyclases (DGC) in Y. pestis, are responsible for the synthesis of c-di-GMP. Y3730, 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 (y3729-31), 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.