CME during aging. CME involves recruitment of adaptors, scaffolds, and clathrin during a “variable” phase, whose timing likely depends on cargo. Actin, myosins, and scission effectors arrive in a shorter, regular phase of predictable duration, generating a coated vesicle. During aging, H⁺ ATPase Pma1 accumulation leads to elevated cytoplasmic pH, V-ATPase disassembly, and increased vacuolar pH that inhibits TORC1 signaling. With reduced TORC1 signaling, the kinase Npr1 phosphorylates endocytic factors such as α-arrestins to inhibit their activity. This could ultimately delay endocytosis by reducing cargo ubiquitination and loading into vesicles, causing the prolonged variable phase of endocytosis observed in old mother cells.