The GATC-binding protein SeqA is required for bile resistance and virulence in Salmonella enterica serovar typhimurium.

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.