Affiliation:
1. Department of Molecular Biology and Immunology
2. Department of Pathology and Anatomy University of North Texas Health Science Center at Fort Worth, Fort Worth, Texas 76107-2699
Abstract
ABSTRACT
The predominant mode of growth of bacteria in the environment is within sessile, matrix-enclosed communities known as biofilms. Biofilms often complicate chronic and difficult-to-treat infections by protecting bacteria from the immune system, decreasing antibiotic efficacy, and dispersing planktonic cells to distant body sites. While the biology of bacterial biofilms has become a major focus of microbial research, the regulatory mechanisms of biofilm development remain poorly defined and those of dispersal are unknown. Here we establish that the RNA binding global regulatory protein CsrA (carbon storage regulator) of
Escherichia coli
K-12 serves as both a repressor of biofilm formation and an activator of biofilm dispersal under a variety of culture conditions. Ectopic expression of the
E. coli
K-12
csrA
gene repressed biofilm formation by related bacterial pathogens. A
csrA
knockout mutation enhanced biofilm formation in
E. coli
strains that were defective for extracellular, surface, or regulatory factors previously implicated in biofilm formation. In contrast, this
csrA
mutation did not affect biofilm formation by a
glgA
(glycogen synthase) knockout mutant. Complementation studies with
glg
genes provided further genetic evidence that the effects of CsrA on biofilm formation are mediated largely through the regulation of intracellular glycogen biosynthesis and catabolism. Finally, the expression of a chromosomally encoded
csrA
′
-
′
lacZ
translational fusion was dynamically regulated during biofilm formation in a pattern consistent with its role as a repressor. We propose that global regulation of central carbon flux by CsrA is an extremely important feature of
E. coli
biofilm development.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
356 articles.
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