Journal
JOURNAL OF BACTERIOLOGY
Volume 189, Issue 23, Pages 8496-8502Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.01156-07
Keywords
-
Categories
Ask authors/readers for more resources
Disruption of the seqA gene of Salmonella enterica serovar Typhimurium causes defects similar to those described in E. coli: filament formation, aberrant nucleoid segregation, induction of the SOS response, envelope instability, and increased sensitivity to membrane-damaging agents. Differences between SeqA(-) mutants of E. coli and S. enterica, however, are found. SeqA(-) mutants of S. enterica form normal colonies and do not exhibit alterations in phage plaquing morphology. Lack of SeqA causes attenuation of S. enterica virulence by the oral route but not by the intraperitoneal route, suggesting a virulence defect in the intestinal stage of infection. However, SeqA(-) mutants are fully proficient in the invasion of epithelial cells. We hypothesize that attenuation of SeqA(-) mutants by the oral route may be caused by bile sensitivity, which in turn may be a consequence of envelope instability.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available