Lon Chubiz, PhD
Final Abstract for URS Program
The mar-sox-rob regulon has been implicated in transcriptional regulation of several stress responses, such efflux of antibiotics, enzymes that break down reactive oxygen species, repression of biofilm formation, or repression of motility through downregulation of flagellar expression. This system is conserved among enteric bacteria and has been studied in species, such as E. coli and S. typhimurium. Some of these mechanisms can be costly and slow cell growth while increasing the probability of survival through tolerance of toxic environments. SoxS works in coordination with SoxR to respond to redox stress encountered by the cell. Interestingly, the overexpression of SoxS in Salmonella, which may be due to some costly mechanism activated by SoxS. The exact identity of such a mechanism remains unknown. This study attempts to identify regions controlled by SoxS that are slowing growth through transposon mutagenesis in an inducible SoxS overexpression mutant. The inducible SoxS gene and transposon were transformed into the cell via electroporation. The mutants yielded from electroporation were then enriched for faster growing phenotypes using serially diluted culture. Mutants were then isolated from this culture and kinetically assayed for increased growth over the original, overexpression mutant. Kinetic assays are ongoing. Once mutants with increased growth patterns are identified and it is confirmed that the transposon is the cause of this increased growth, the mutants will be sequenced to identify genes that slow growth in the overexpression of SoxS.