Glucose Stress Response Through the PKA-Msn2 Axis in Saccharomyces cerevisiae
Cellular adaption to glucose availability requires precise coordination between signaling pathways and gene expression. In Saccharomyces cerevisiae, the vacuole serves as a metabolic hub whose protein composition and activity are dynamically regulated to nutrient availability. Additionally, the Protein Kinase A (PKA) pathway is a central mediator of glucose stress response, acting through the transcriptional factor Msn2. However, how PKA-Msn2 axis connects environmental cues to vacuolar gene expression remains poorly understood. In this study, we investigate how PKA regulates Msn2 subcellular localization and its impact on expression of PRC1, a representative vacuolar lumenal hydrolase. By combining Msn2 subcellular localization and gene expression analysis, we found glucose limitation induces PRC1 expression, which reduced after deletion of Msn2/4 and disruption of Stress Response Elements (STRE) in PRC1 promoter. Furthermore, reduced PKA activity is associated with nuclear accumulation of Msn2 and enhanced PRC1 expression, whereas deletion of Msn2/4 attenuates this effect. Results reveal that PKA-mediated regulation of Msn2 is essential for glucose stress responses and provide insight into how signaling pathways control PRC1 expression in yeast.