Electron transport chain disruption leads to failure of glucose derepression via the Snf1/AMPK pathway

When Saccharomyces cerevisiae cells transition from a glucose-rich environment to low glucose conditions, the expression of genes that were previously repressed by glucose is derepressed, enabling the cell to adapt metabolic processes to the available carbon source. The Snf1 pathway is one of the primary signaling pathways responsible for orchestrating glucose sensing and signaling. In this study, we investigate the impact of disrupted electron transport chain (ETC) function, a mitochondrial protein complex essential for respiratory energy generation, in glucose derepression. We observe that respiratory incompetent mutants exposed to glucose are unable to subsequently utilize galactose as a carbon source in minimal media. In contrast, ETC mutants that have been generated and maintained on galactose can effectively continue to metabolize galactose until glucose exposure. We define this phenomenon as a F ailure of G lucose D erepression (FGD), wherein respiratory incompetent cells fail to fully reverse glucose repressed gene expression regulation. Through further characterization, we show how irregular localization patterns of crucial proteins within the Snf1 pathway are associated with FGD suggesting a potential novel connection between the ETC and the Snf1 pathway during carbon source transition.