Mga/RofA-like proteins are emerging class of transcription regulators that regulates virulence traits in pathogenic members of Bacillota (e.g. Streptococcus, Enterococcus, Bacillus anthracis). Their activities are thought to be modulated through phosphorylation, however the precise mechanisms are unknown. We have recently identified a Mga/RofA-like protein, GadR, in the important food-borne pathogen Listeria monocytogenes. GadR controls the expression of glutamate decarboxylase system (GadT2D2) and thereby regulates acid resistance, which determines gastric survival. Interestingly, GadR activates gadT2D2 in rich media (brain heart infusion) but not in nutrient limited conditions such as minimum media (MM). Herein, we sought to understand how acid resistance is repressed in MM. For this, we engineered L. monocytogenes mutant stains by redirecting the sole trehalose metabolism operon treBA under the control of PgadT2D2, thus coupling trehalose assimilation with PgadT2D2 activity. These mutant strains cannot grow in MM with trehalose supplied as a sole carbon source (MM-tre), confirming that PgadT2D2 is inactive under nutrient limited conditions. Suppressors that restored growth in MM-tre acquired mutations in PgadT2D2 or duplicated treBA operon. Interestingly, suppressor mutants are found from mutant strains already carrying codY mutations. On-going investigations are characterising how these mutations affect gadT2D2 expression and acid resistance. These results will give insights on the regulatory mechanisms of virulence traits modulated by Mga/RofA-like proteins, inform food formulation to improve food safety, and potentially provide novel strategies for anti-virulence therapies development.