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Salmonella enterica is a foodborne pathogen that causes gastroenteritis, leading to approximately 19,000 hospitalizations and 380 deaths each year in the United States. Current efforts to develop new drugs aim to disrupt pathways important to the bacteria's fitness during infection. High throughput genetic screening of Salmonella mutants that are less fit in mice has identified the fra locus, containing the fraBDAE operon, which confers the ability to metabolize fructose-asparagine (F-Asn). Disruption of this pathway, specifically of fraB, is bacteriostatic in the presence of F-Asn and causes a significant decrease in Salmonella fitness in mice. The observed phenotype is hypothesized to be due to an accumulation of the toxic intermediate 6-phosphofructose-aspartate (6-P-F-Asp). This has been supported by genetics and mass spectroscopy. Our goal was to better understand the mechanism of this toxicity, which has not yet been examined. To do so, a library of T-POP transposon insertions was created in a fraB mutant background. Mutants were then selected that could grow in minimal media with glucose and F-Asn. Several mutants were isolated and classified to identify gene products that alleviate the toxicity of F-Asn to fraB mutants.