Affiliation:
1. Department of Microbiology and Molecular Genetics and Shipley Institute of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Abstract
ABSTRACT
The toxin-coregulated pilus (TCP) of
Vibrio cholerae
is essential for colonization. It was recently reported that
rfb
mutations in
V. cholerae
569B cause the translocation arrest of the structural subunit of TCP, raising the possibility that the colonization defects of lipopolysaccharide mutants are due to effects on TCP biogenesis. However, an
rfbB
gene disruption in either
V. cholerae
O395 or 569B has no apparent effect on surface TCP production as assessed by immunoelectron microscopy and CTX phage transduction, and an
rfbD
::Tn
5lac
mutant of O395 also shows no defect in TCP expression. We conclude that the colonization defect associated with
rfb
mutations is unrelated to defects in TCP assembly.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
48 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献