Early responses to hyperosmotic stress at the yeast vacuole.

ABSTRACT: In yeast, early adaptation to hyperosmotic stress involves organelle-based mechanisms, including synthesis of phosphatidylinositol 3,5-bisphosphate (PI(3,5)P₂) at the vacuole. This low-level signaling lipid drives vacuolar fragmentation and activates the V-ATPase proton pump, which acidifies the vacuole and drives salt sequestration. The vacuole-resident V-ATPase subunit Vph1 interacts with PI(3,5)P₂ via its N-terminal domain (Vph1NT), directly linking lipid signaling to proton pump regulation. Under NaCl stress, PI(3,5)P₂ rapidly accumulates, triggering increased V-ATPase activity and vacuolar remodeling; these responses are impaired by deficient PI(3,5)P₂ synthesis. A Vph1NT-GFP fusion protein with no membrane domain is cytosolic without salt,

SUBMITTER: Saravanan K 

PROVIDER: S-EPMC12363888 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature