Zhao Tianhu, Lei Fanglin, Zhang Zhenyu, Wang Di, Ma Luyan Z
State Key Laboratory of Microbial Resources, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
College of Life Sciences, University of Chinese Academy of Sciences, No. 1 Yanqihu East Rd, Huairou District, Beijing 101408, PR China.
ISME J. 2025 Jan 2;19(1). doi: 10.1093/ismejo/wraf038.
The biofilm matrix primarily consists of proteins, exopolysaccharides, and extracellular DNA. Pseudomonas aeruginosa aminopeptidase is one of the most abundant matrix proteins in P. aeruginosa biofilms and plays a crucial role in modulating biofilm development. In a previous study, we have revealed that the loss of aminopeptidase enhances the attachment ability of P. aeruginosa. However, the mechanism by which aminopeptidase affects attachment remains unclear. In this study, we demonstrate that aminopeptidase is the primary protein associated with the matrix exopolysaccharide Psl. The loss of aminopeptidase leads to increased production of Psl, resulting in enhanced attachment of P. aeruginosa. Further investigation shows that aminopeptidase represses the transcription of the psl operon through the LasI/LasR quorum-sensing system, rather than via other known psl regulators or the cyclic-di-GMP signaling molecule. Aminopeptidase inhibits the transcription of lasI via the short peptides cleaved from the proform of aminopeptidase during its activation, which results in reduced biosynthesis of the quorum-sensing signaling molecule, N-(3-oxododecanoyl)-L-homoserine lactone, further decreasing the production of Psl. In conclusion, our study reveals an interplay between two key matrix components via quorum-sensing signal, suggesting a mechanism by which bacteria control initial attachment and exopolysaccharide production in response to cell density.
生物膜基质主要由蛋白质、胞外多糖和细胞外DNA组成。铜绿假单胞菌氨肽酶是铜绿假单胞菌生物膜中最丰富的基质蛋白之一,在调节生物膜形成过程中起关键作用。在先前的一项研究中,我们发现氨肽酶的缺失增强了铜绿假单胞菌的附着能力。然而,氨肽酶影响附着的机制仍不清楚。在本研究中,我们证明氨肽酶是与基质胞外多糖Psl相关的主要蛋白质。氨肽酶的缺失导致Psl产量增加,从而增强了铜绿假单胞菌的附着。进一步研究表明,氨肽酶通过LasI/LasR群体感应系统抑制psl操纵子的转录,而不是通过其他已知的psl调节因子或环二鸟苷酸信号分子。氨肽酶在激活过程中通过从氨肽酶前体形式切割的短肽抑制lasI的转录,这导致群体感应信号分子N-(3-氧代十二烷酰基)-L-高丝氨酸内酯的生物合成减少,进而降低Psl的产生。总之,我们的研究揭示了通过群体感应信号两种关键基质成分之间的相互作用,提示了一种细菌响应细胞密度控制初始附着和胞外多糖产生的机制。