Chang Jingyang, Zhou Yining, Zhang Miaomiao, Li Xue, Zhang Nan, Luo Xi, Ni Bin, Lu Renfei, Zhang Yiquan
Department of Clinical Laboratory, Nantong Third People's Hospital, Affiliated Nantong Hospital 3 of Nantong University, Nantong, Jiangsu, China.
Department of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Appl Environ Microbiol. 2025 Sep 11:e0072425. doi: 10.1128/aem.00724-25.
, the leading cause of seafood-associated gastroenteritis, often exists in a biofilm state. Biofilm formation in this bacterium is regulated by a complex network of factors, including the second messenger c-di-GMP. CalR, a LysR-type transcriptional regulator, has been demonstrated to play a role in regulating the expression of virulence genes and swarming motility of . In this study, we demonstrate that CalR positively regulates biofilm formation by enhancing the production of exopolysaccharides (EPSs), extracellular proteins, extracellular DNA (eDNA), and c-di-GMP. RNA sequencing reveals that CalR regulates the transcription of 167 genes, including those potentially involved in c-di-GMP metabolism (e.g., , , and ) and biofilm-associated regulators (e.g., ). CalR directly suppresses the transcription of , , and while activating transcription in a direct manner. Additionally, CalR directly activates the transcription of but indirectly activates that of , both of which are involved in EPS production. In summary, these findings elucidate the regulatory mechanisms by which CalR promotes biofilm formation in and highlight its role in modulating c-di-GMP homeostasis and biofilm matrix production. This work enhances our understanding of the regulatory network governing biofilm formation by .IMPORTANCEBiofilm formation is a critical survival strategy for , allowing it to persist in adverse environments. Understanding the regulatory mechanisms underlying biofilm formation is essential for developing strategies to control infections caused by this pathogen. This work demonstrates that CalR positively regulates the production of EPS, extracellular proteins, and eDNA, as well as biofilm formation by . CalR regulates the global gene expression in , including genes such as , , , and . ScrP negatively impacts biofilm formation, whereas , , and contribute to c-di-GMP metabolism. CalR represses , , and while activating and also promotes the production of c-di-GMP. These findings indicate how CalR positively regulates biofilm formation by .
作为海鲜相关肠胃炎的主要病因，通常以生物膜状态存在。该细菌中的生物膜形成受包括第二信使环二鸟苷酸（c-di-GMP）在内的复杂因子网络调控。CalR是一种LysR型转录调节因子，已被证明在调节毒力基因表达和的群体运动中发挥作用。在本研究中，我们证明CalR通过增强胞外多糖（EPS）、胞外蛋白、胞外DNA（eDNA）和c-di-GMP的产生来正向调节生物膜形成。RNA测序显示CalR调节167个基因的转录，包括那些可能参与c-di-GMP代谢（如、和）以及生物膜相关调节因子（如）的基因。CalR直接抑制、和的转录，同时直接激活的转录。此外，CalR直接激活的转录，但间接激活参与EPS产生的的转录。总之，这些发现阐明了CalR促进生物膜形成的调控机制，并突出了其在调节c-di-GMP稳态和生物膜基质产生中的作用。这项工作增进了我们对生物膜形成调控网络的理解。重要性生物膜形成是生存的关键策略，使其能够在不利环境中持续存在。了解生物膜形成的调控机制对于制定控制该病原体引起感染的策略至关重要。这项工作表明CalR正向调节EPS、胞外蛋白和eDNA的产生以及生物膜形成。CalR调节中的全局基因表达，包括、、和等基因。ScrP对生物膜形成有负面影响，而、和则参与c-di-GMP代谢。CalR抑制、和，同时激活并促进c-di-GMP的产生。这些发现表明CalR如何正向调节生物膜形成。
