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Journal of Bacteriology, December 2007, p. 8496-8502, Vol. 189, No. 23
0021-9193/07/$08.00+0 doi:10.1128/JB.01156-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
,
Marcello Jakomin,1
Ignacio Segura,1
M. Graciela Pucciarelli,2
Francisco Ramos-Morales,1
Francisco García-del Portillo,2 and
Josep Casadesús1*
Departamento de Genética, Facultad de Biología, Universidad de Sevilla, Apartado 1095, Sevilla 41080,1 Departamento de Biotecnología Microbiana, Centro Nacional de Biotecnología, CSIC, Campus de Cantoblanco, 28049 Madrid, Spain2
Received 21 July 2007/ Accepted 14 September 2007
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.
Published ahead of print on 28 September 2007.
Supplemental material for this article may be found at http://jb.asm.org/.
Present address: Department of Pathology, Cambridge University, Tennis Court Road, Cambridge CB2 1QP, England.
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