A starvation-induced regulator, RovM, acts as a switch for planktonic/biofilm state transition in Yersinia pseudotuberculosis.
A starvation-induced regulator, RovM, acts as a switch for planktonic/biofilm state transition in Yersinia pseudotuberculosis.
复制标题
饥饿诱导的调节因子 RovM 在假结核耶尔森氏菌中充当浮游/生物膜状态转换的开关
DOI：
10.1038/s41598-017-00534-9
复制
发表时间：
2017-04-04
影响因子：
4.6
通讯作者：
Shen X
中科院分区：
文献类型：
--
作者：
Zhao R;Song Y;Dai Q;Kang Y;Pan J;Zhu L;Zhang L;Wang Y;Shen X
浮游状态和生物膜相关状态之间的转变是病原菌的关键发育决定。鼠疫耶尔森氏菌的生物膜形成受其跳蚤载体和体外的 hmsHFRS 基因（β-1, 6-N-乙酰基-D-葡萄糖胺合成操纵子）的调节。然而，假结核耶尔森菌生物膜形成的机制仍不清楚。在这项研究中，我们证明了 LysR 型调节因子 RovM 通过充当这两个功能的转录调节因子，反向调节假结核菌中的生物膜形成和运动。 RovM 在基本培养基中生长过程中受到强烈诱导，但在复杂培养基中受到强烈抑制。一方面，RovM 通过识别 flhDC 启动子上游的操纵子来激活 FlhDC（鞭毛基因的主调节因子）的表达，从而增强细菌运动性。另一方面，RovM 在营养有限的条件下抑制 β-GlcNAc 的产生，通过直接结合 hmsHFRS 启动子的 -35 元件来负向调节 hmsHFRS 的表达。与野生型细菌相比，rovM 突变体建立了更致密的生物膜，并导致小鼠和蚕幼虫更广泛的死亡。这些结果表明，RovM 作为分子开关来协调参与生物膜形成和运动的基因表达，以响应营养物质的可用性。
The transition between the planktonic state and the biofilm-associated state is a key developmental decision for pathogenic bacteria. Biofilm formation by Yersinia pestis is regulated by hmsHFRS genes (β-1, 6-N-acetyl-D-glucosamine synthesis operon) in its flea vector and in vitro. However, the mechanism of biofilm formation in Yersinia pseudotuberculosis remains elusive. In this study, we demonstrate that the LysR-type regulator RovM inversely regulates biofilm formation and motility in Y. pseudotuberculosis by acting as a transcriptional regulator of these two functions. RovM is strongly induced during growth in minimal media but strongly repressed in complex media. On one hand, RovM enhances bacterial motility by activating the expression of FlhDC, the master regulator of flagellar genes, via the recognition of an operator upstream of the flhDC promoter. On the other hand, RovM represses β-GlcNAc production under nutrition-limited conditions, negatively regulating hmsHFRS expression by directly binding to the −35 element of its promoter. Compared to wild-type bacteria, the rovM mutant established denser biofilms and caused more extensive mortality in mice and silkworm larvae. These results indicate that RovM acts as a molecular switch to coordinate the expression of genes involved in biofilm formation and motility in response to the availability of nutrients.