Faculty Sponsor
Lon Chubiz
Final Abstract for URS Program
Salicylate, a topical antiseptic and non-steroidal anti-inflammatory drug (NSAID), is known to induce physiological stress adaptation in bacteria. One such adaptation involves the cyclopropanation of unsaturated membrane fatty acids, a process that enhances membrane integrity under stress conditions. In Salmonella enterica serovar Typhimurium 14028S, the cfa gene encodes cyclopropane fatty acid synthase, a key enzyme that modifies membrane lipids to promote stress tolerance. To understand regulatory mechanisms underlying salicylate induction of cfa expression, a lacZ reporter system was employed to screen a library of transposon mutants for altered cfa promoter activity. Mutant 243 showed a pronounced 5-8 fold decrease in cfa activity compared to the wild-type during salicylate treatment. Gas chromatography analysis confirmed that this mutant had impaired conversion of unsaturated to cyclopropane fatty acids. Whole-genome sequencing further revealed disruption of the nirBCD-cysG operon in mutant 243. These findings indicate that the nirBCDcysG operon may contribute to salicylate-dependent cfa expression and membrane lipid remodeling in Salmonella.
Presentation Type
Visual Presentation
Document Type
Article