随着细菌耐药性问题日益突出，对病原细菌生物膜形成的调控机制和信号途径研究已经成为当前微生物领域的研究热点之一。本项目在前期对假结核耶尔森氏菌生物膜形成调控机制研究工作基础上，初步提出一个CsrA-RovM双重分子开关在转录水平和转录后水平同时反向调控细菌生物膜形成和运动性相关基因表达的双重调控机制模型，本项目将在完善该模型的基础上，进一步深入揭示CsrA-RovM双重分子开关在饥饿条件下通过抑制细菌生物膜形成，同时激活细菌鞭毛生成而增强细菌运动性以促进细菌觅食或生物膜分散的独特调控机制，揭示其响应饥饿的信号传递途经及该调控开关的生理意义，并揭示其调控作用的广泛性。通过本项目的实施，将不仅在理论上大幅提升对细菌生物膜形成过程和调控机制的认识，填补对饥饿起始状态下细菌进入觅食状态，以及生物膜分散进入浮游状态这两个阶段调控机制研究的空白，并可能为控制细菌生物膜提供新的可行途径。

As bacterial resistance to antibiotics has become increasingly prominent, revealing the regulatory mechanisms and signaling pathways of biofilm formation in pathogenic bacteria has become one of the hotspots in the field of microbiological research. Based on our previously studies on the regulatory mechanisms of biofilm formation in Yersinia pseudotuberculosis, we proposed a novel regulatory model in which the double-tier molecular switch CsrA-RovM positively regulates bacterial biofilm related gene expression post-transcriptionally and negatively regulates motility gene expression transcriptionally. In this project, we will first refine this model, and then we will reveal the unique regulatory mechanism of the CsrA-RovM switch in inhibiting bacterial biofilm formation while activating bacterial flagella production for promoting foraging bacteria formation and biofilm dispersion under starvation conditions. We will also reveal the signal transduction pathways, physiological significance and the broad regulatory roles of the CsrA-RovM molecular switch. Through the implementation of this project, we will not only greatly enhance the understanding of regulation mechanisms of bacterial biofilm formation, foraging bacteria formation and biofilm dispersion, and may also provide a new way to control bacterial biofilm.