The Gram-negative bacterium adapts to changes in the environment by selectively producing the necessary machinery to take up and metabolize available carbohydrates. The import of fructose by the fructose-specific phosphoenolpyruvate (PEP) phosphotransferase system (PTS) is of particular interest because of its putative connection to cholera pathogenesis and persistence. Here, we describe the expression and regulation of , which encodes an EIIA-FPr fusion protein as part of the fructose-specific PTS in Using a series of transcriptional reporter fusions and additional biochemical and genetic assays, we identified Cra (catabolite repressor/activator) and cAMP receptor protein (CRP) as regulators of expression and determined that this regulation is dependent upon the presence or absence of PTS sugars. Cra functions as a repressor, downregulating expression in the absence of fructose when components of PTS are not needed. CRP functions as an activator of expression. We also report that Cra and CRP can affect expression independently; however, CRP can modulate expression in the presence of fructose and glucose. Evidence from this work provides the foundation for continued investigations into PTS and its relationship to the life cycle. is the causative agent of cholera disease. While current treatments of care are accessible, we still lack an understanding of the molecular mechanisms that allow to survive in both aquatic reservoirs and the human small intestine, where pathogenesis occurs. Central to 's survival is its ability to use available carbon sources. Here, we investigate the regulation of , which encodes a protein central to the import and metabolism of fructose. We show that expression is controlled by the transcriptional regulators Cra and CRP. This work contributes toward a clearer understanding of how carbon source availability impacts the physiology and, potentially, the persistence of the pathogen.