期刊
MOLECULAR MICROBIOLOGY
卷 39, 期 2, 页码 223-235出版社
WILEY
DOI: 10.1046/j.1365-2958.2001.02195.x
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资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [K08AI001588, R01AI043486] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM058213] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI043486, K08 AI001588-01, K08 AI01588, AI43486] Funding Source: Medline
- NIGMS NIH HHS [GM58213, R01 GM058213] Funding Source: Medline
Throughout most of history, epidemic and pandemic cholera was caused by Vibrio cholerae of the serogroup O1. In 1992, however, a V. cholerae strain of the serogroup O139 emerged as a new agent of epidemic cholera. Interestingly, V. cholerae O139 forms biofilms on abiotic surfaces more rapidly than V. cholerae O1 biotype El Tor, perhaps because regulation of exopolysaccharide synthesis in V. cholerae O139 differs from that in O1 El Tor. Here, we show that all flagellar mutants of V. cholerae O139 have a rugose colony morphology that is dependent on the vps genes. This suggests that the absence of the flagellar structure constitutes a signal to increase exopolysaccharide synthesis. Furthermore, although exopolysaccharide production is required for the development of a three-dimensional biofilm, inappropriate exopolysaccharide production leads to inefficient colonization of the infant mouse intestinal epithelium by flagellar mutants. Thus, precise regulation of exopolysaccharide synthesis is an important factor in the survival of V. cholerae O139 in both aquatic environments and the mammalian intestine.
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