FIGURE 2.

V-ATPase in non-vacuolar organelles (Stv1p-containing complexes) plays a yet unknown role in C. albicans virulence. Wild-type: When functional, V-ATPase-mediated acidification of vacuoles, Golgi, and secretory vesicles maintains organelle pH and supports traffic of Pma1p to the cell surface for proton efflux and maintenance of an alkaline cytosol. VPH1 deficient: C. albicans grows normally at neutral pH when only Vph1p-containing V-ATPase complexes (vacuolar membrane) are missing. Only modest filamentation defects are obvious, despite the concomitant vacuolar alkalinization and defective Pma1p activity (Raines et al., 2013 and unpublished results). VMA3 deficient: Vacuolar alkalinization and defective Pma1p activity occur at levels equal to that of VPH1 deficient cells when all V-ATPase function is missing (Stv1p- and Vph1-containing V-ATPase complexes; Rane et al., 2013 and unpublished results). However, VMA3 deficient C. albicans exhibits growth defects at neutral pH and severely reduced filamentation under these conditions. We therefore hypothesize that the presence of Stv1p-containing V-ATPase in non-vacuolar organelles maintains virulence in the face of defective vacuolar and cytoplasmic pH homeostasis. Pink = acidic/acidified, blue = alkaline/alkalinized.