This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Xiong, X. Articles by Misra, R. Search for Related Content PubMed PubMed Citation Articles by Xiong, X. Articles by Misra, R.

 Previous Article  |  Next Article 

J. Bacteriol., Feb 1996, 1213-1215, Vol 178, No. 4
Copyright © 1996, American Society for Microbiology

Assembly-defective OmpC mutants of Escherichia coli K-12

X Xiong, JN Deeter and R Misra
Department of Microbiology, Arizona State University, Tempe 85287-2701, USA.

Novel ompC(Dex) alleles were utilized to isolate mutants defective in OmpC biogenesis. These ompC(Dex) alleles also conferred sensitivity to sodium dodecyl sulfate (SDS), which permitted the isolation of SDS- resistant and OmpC-specific phage-resistant mutants that remained Dex+. Many mutants acquired resistance against these lethal agents by lowering the OmpC level present in the outer membrane. In the majority of these mutants, a defect in the assembly (metastable to stable trimer formation) was responsible for lowering OmpC levels. The assembly defects in various mutant OmpC proteins were caused by single-amino- acid substitutions involving the G-39, G-42, G-223, G-224, Q-240, G- 251, and G-282 residues of the mature protein. This assembly defect was correctable by an assembly suppressor allele, asmA3. In addition, we investigated one novel OmpC mutant in which an assembly defect was caused by a disulfide bond formation between two nonnative cysteine residues. The assembly defect was fully corrected in a genetic background in which the cell's ability to form disulfide bonds was compromised. The assembly defect of the two-cysteine OmpC protein was also mended by asmA3, whose suppressive effect was not achieved by preventing disulfide bond formation in the mutant OmpC protein.

This article has been cited by other articles:

• Prieto, A. I., Hernandez, S. B., Cota, I., Pucciarelli, M. G., Orlov, Y., Ramos-Morales, F., Garcia-del Portillo, F., Casadesus, J. (2009). Roles of the Outer Membrane Protein AsmA of Salmonella enterica in the Control of marRAB Expression and Invasion of Epithelial Cells. J. Bacteriol. 191: 3615-3622 [Abstract] [Full Text]  
• Tanji, Y., Hattori, K., Suzuki, K., Miyanaga, K. (2008). Spontaneous Deletion of a 209-Kilobase-Pair Fragment from the Escherichia coli Genome Occurs with Acquisition of Resistance to an Assortment of Infectious Phages. Appl. Environ. Microbiol. 74: 4256-4263 [Abstract] [Full Text]  
• Castillo-Keller, M., Vuong, P., Misra, R. (2006). Novel Mechanism of Escherichia coli Porin Regulation. J. Bacteriol. 188: 576-586 [Abstract] [Full Text]  
• CastilloKeller, M., Misra, R. (2003). Protease-Deficient DegP Suppresses Lethal Effects of a Mutant OmpC Protein by Its Capture. J. Bacteriol. 185: 148-154 [Abstract] [Full Text]  
• Kloser, A. W., Reading, J. T., McDermott, T., Stidham, R., Misra, R. (2001). Intragenic Suppressors of an OmpF Assembly Mutant and Assessment of the Roles of Various OmpF Residues in Assembly through Informational Suppressors. J. Bacteriol. 183: 264-269 [Abstract] [Full Text]  
• Misra, R., CastilloKeller, M., Deng, M. (2000). Overexpression of Protease-Deficient DegPS210A Rescues the Lethal Phenotype of Escherichia coli OmpF Assembly Mutants in a degP Background. J. Bacteriol. 182: 4882-4888 [Abstract] [Full Text]  
• Berlyn, M. K. B. (1998). Linkage Map of Escherichia coli K-12, Edition 10: The Traditional Map. Microbiol. Mol. Biol. Rev. 62: 814-984 [Abstract] [Full Text]