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Exopolysaccharides amylovoran and levan contribute to sliding motility in the fire blight pathogen Erwinia amylovora.

Authors :
Yuan X
Eldred LI
Sundin GW
Source :
Environmental microbiology [Environ Microbiol] 2022 Oct; Vol. 24 (10), pp. 4738-4754. Date of Electronic Publication: 2022 Sep 15.
Publication Year :
2022

Abstract

Erwinia amylovora, the causative agent of fire blight, uses flagella-based motilities to translocate to host plant natural openings; however, little is known about how this bacterium migrates systemically in the apoplast. Here, we reveal a novel surface motility mechanism, defined as sliding, in E. amylovora. Deletion of flagella assembly genes did not affect this movement, whereas deletion of biosynthesis genes for the exopolysaccharides (EPSs) amylovoran and levan resulted in non-sliding phenotypes. Since EPS production generates osmotic pressure that potentially powers sliding, we validated this mechanism by demonstrating that water potential positively contributes to sliding. In addition, no sliding was observed when the water potential of the surface was lower than -0.5 MPa. Sliding is a passive motility mechanism. We further show that the force of gravity plays a critical role in directing E. amylovora sliding on unconfined surfaces but has a negligible effect when cells are sliding in confined microcapillaries, in which EPS-dependent osmotic pressure acts as the main force. Although amylovoran and levan are both required for sliding, we demonstrate that they exhibit different roles in bacterial communities. In summary, our study provides fundamental knowledge for a better understanding of mechanisms that drive bacterial sliding motility.<br /> (© 2022 The Authors. Environmental Microbiology published by Society for Applied Microbiology and John Wiley & Sons Ltd.)

Details

Language :
English
ISSN :
1462-2920
Volume :
24
Issue :
10
Database :
MEDLINE
Journal :
Environmental microbiology
Publication Type :
Academic Journal
Accession number :
36054324
Full Text :
https://doi.org/10.1111/1462-2920.16193