Departamento de Microbiología, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, CONICET, Rosario, Argentina.
Interfaculty Institute for Genetics and Functional Genomics, Department of Functional Genomics, University Medicine Greifswald, Greifswald, Germany.
J Bacteriol. 2018 Dec 20;201(2). doi: 10.1128/JB.00473-18. Print 2019 Jan 15.
Bacterial biofilms are important in natural settings, biotechnology, and medicine. However, regulation of biofilm development and its persistence in different niches is complex and only partially understood. One key step during the biofilm life cycle is dispersal, when motile cells abandon the mature biofilm to spread out and colonize new niches. Here, we show that in the model bacterium the general stress transcription factor SigB is essential for halting detrimental overgrowth of mature biofilm and for triggering dispersal when nutrients become limited. Specifically, SigB-deficient biofilms were larger than wild-type biofilms but exhibited accelerated cell death, significantly greater sensitivity to different stresses, and reduced dispersal. Interestingly, the signal detected by SigB to limit biofilm growth was transduced through the RsbP-dependent metabolic arm of the SigB regulatory cascade, which in turn positively controlled expression of SinR, the master regulator of biofilm formation and cell motility. This novel SigB-SinR regulatory circuit might be important in controlling the fitness of biofilms (either beneficial or harmful) in diverse environments. Biofilms are crucial for bacterial survival, adaptation, and dissemination in natural, industrial, and medical systems. Sessile cells embedded in the self-produced extracellular matrix of the biofilm benefit from a division of labor and are protected from environmental insults. However, as the biofilm ages, cells become stressed because of overcrowding, starvation, and accumulation of waste products. How does the sessile biofilm community sense and respond to stressful conditions? Here, we show that in , the transcription factors SigB and SinR control whether cells remain in or leave a biofilm when metabolic conditions become unfavorable. This novel SigB-SinR regulatory circuit might be important for controlling the fitness of biofilms (either beneficial or harmful) in diverse environments.
细菌生物膜在自然环境、生物技术和医学中都很重要。然而,生物膜的发展和在不同小生境中的持续存在的调节是复杂的,并且只是部分理解。生物膜生命周期中的一个关键步骤是分散,即运动细胞放弃成熟的生物膜,扩散并殖民新的小生境。在这里,我们表明在模式细菌 中,一般应激转录因子 SigB 对于阻止成熟生物膜的过度生长和在营养物质有限时触发分散是必不可少的。具体来说,SigB 缺陷型生物膜比野生型生物膜大,但表现出加速的细胞死亡、对不同应激的显著更大敏感性和减少的分散。有趣的是,SigB 检测到的限制生物膜生长的信号是通过 SigB 调节级联的 RsbP 依赖代谢臂转导的,这反过来又正向控制了生物膜形成和细胞运动的主调节剂 SinR 的表达。这种新型的 SigB-SinR 调节回路可能在控制生物膜(有益或有害)在不同环境中的适应性方面很重要。生物膜对于细菌在自然、工业和医疗系统中的生存、适应和传播至关重要。嵌入生物膜自身产生的细胞外基质中的不动细胞受益于分工,并免受环境伤害。然而,随着生物膜的老化,由于过度拥挤、饥饿和废物积累,细胞会受到压力。不动生物膜群落如何感知和应对压力条件?在这里,我们表明在 中,转录因子 SigB 和 SinR 控制细胞在代谢条件不利时是留在生物膜中还是离开生物膜。这种新型 SigB-SinR 调节回路可能在控制生物膜(有益或有害)在不同环境中的适应性方面很重要。