Molecular Mechanism of Vibrio cholerae biofilm adhesion

Abstract

Biofilms are communities of microorganisms that play a significant role as virulence factors in disease transmission. The ability to attach to surfaces is an important feature which facilitates both host colonization and survival in the environment. To attach to a wide array of biotic and abiotic surfaces, biofilm‐dwelling bacterial cells need to produce specific adhesion molecules. The causative agent of pandemic cholerae, Vibrio cholerae, forms biofilms dependent on Vibrio polysaccharide (VPS), the primary component of the biofilm matrix, which makes a significant contribution to the structural integrity of the biofilm. In addition to VPS, the biofilm matrix contains proteins and nucleic acids; together these components play an important role in maintaining the integrity of the biofilm. The three main proteins of the biofilm matrix are RbmA, RbmC and Bap1. In this study we focus on RbmC and Bap1, which are considered adhesion proteins with overlapping but distinct functions. Both proteins share sequence identity and core structural features: a β‐propeller domain, and a β‐prism domain. RbmC contains two functional β‐prism domains which bind with high affinity to the core of complex N‐glycans, while Bap1 has only one domain which appears to have lost the ability to bind glycans. Our study finds that the two adhesins differ in the adhesive properties of the β‐prism domains that interface with the external environment. The current study combines insights from prior crystallographic work with functional assays in V. cholerae biofilms to demonstrate the modular nature of Bap1 and RbmC and how V. cholerae utilizes these two biofilm‐specific adhesins to achieve robust adhesion to various types of surfaces. We also propose a model for how V. cholerae biofilms recognize host surfaces specifically during infection while retaining adhesion to abiotic surfaces. This emphasizes the critical need to develop new biofilm elimination strategies, both from abiotic surfaces and post‐infection as an alternative to antibiotics due to the development of antibiotic resistance.