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核心 cheVAWY 趋化性基因的失活破坏空肠弯曲菌的趋化性运动和有组织的生物膜形成。

Inactivation of the core cheVAWY chemotaxis genes disrupts chemotactic motility and organised biofilm formation in Campylobacter jejuni.

机构信息

Gut Health and Food Safety Programme, Quadram Institute Bioscience, Rosalind Franklin Road, Norwich Research Park, Norwich NR4 7UQ, UK.

Department of Pathology and Infectious Diseases, School of Veterinary Medicine, Faculty of Health and Medical Sciences, University of Surrey, Daphne Jackson Road, Guildford GU2 7AL, UK.

出版信息

FEMS Microbiol Lett. 2020 Jan 15;367(24). doi: 10.1093/femsle/fnaa198.

DOI:10.1093/femsle/fnaa198
PMID:33264398
Abstract

Flagellar motility plays a central role in the bacterial foodborne pathogen Campylobacter jejuni, as flagellar motility is required for reaching the intestinal epithelium and subsequent colonisation or disease. Flagellar proteins also contribute strongly to biofilm formation during transmission. Chemotaxis is the process directing flagellar motility in response to attractant and repellent stimuli, but its role in biofilm formation of C. jejuni is not well understood. Here we show that inactivation of the core chemotaxis genes cheVAWY in C. jejuni strain NCTC 11168 affects both chemotactic motility and biofilm formation. Inactivation of any of the core chemotaxis genes (cheA, cheY, cheV or cheW) impaired chemotactic motility but did not affect flagellar assembly or growth. The ∆cheY mutant swam in clockwise loops, while complementation restored normal motility. Inactivation of the core chemotaxis genes interfered with the ability to form a discrete biofilm at the air-media interface, and the ∆cheY mutant displayed reduced dispersal/shedding of bacteria into the planktonic fraction. This suggests that while the chemotaxis system is not required for biofilm formation per se, it is necessary for organized biofilm formation. Hence interference with the Campylobacter chemotaxis system at any level disrupts optimal chemotactic motility and transmission modes such as biofilm formation.

摘要

鞭毛运动在食源性致病菌空肠弯曲菌中起着核心作用,因为鞭毛运动是弯曲菌到达肠道上皮细胞并随后定植或发病所必需的。鞭毛蛋白也强烈促进传播过程中的生物膜形成。趋化作用是指鞭毛运动响应吸引和排斥刺激的过程,但它在空肠弯曲菌生物膜形成中的作用尚未得到很好的理解。在这里,我们表明空肠弯曲菌菌株 NCTC 11168 中核心趋化作用基因 cheVAWY 的失活会影响趋化运动和生物膜形成。任何核心趋化作用基因(cheA、cheY、cheV 或 cheW)的失活都会损害趋化运动,但不会影响鞭毛组装或生长。cheY 突变体以顺时针环游动,而互补恢复了正常运动。核心趋化作用基因的失活干扰了在气-液界面形成离散生物膜的能力,cheY 突变体显示出细菌向浮游部分分散/脱落的减少。这表明,尽管趋化作用系统本身对于生物膜形成不是必需的,但对于有组织的生物膜形成是必需的。因此,在任何水平上干扰弯曲菌趋化作用系统都会破坏最佳趋化运动和传播模式,如生物膜形成。

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