ArticleMolecular biology of the cell2014
The signaling lipid PI(3,5)P₂ stabilizes V₁-V(o) sector interactions and activates the V-ATPase.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 159 citations in OpenAlex.
- PfATG18 links V-ATPase assembly to endocytic membrane dynamics in malaria parasites.PLoS pathogens · 2026Article
- Spatial organization of phosphoinositide signaling.FEBS letters · 2026Review
- The Lack of a COPII Cargo Receptor Erv14 Impacts Physiological Functions of the Vacuole in Saccharomyces cerevisiae.Traffic (Copenhagen, Denmark) · 2026Article
- Early lipid-mediated responses to hyperosmotic stress at the yeast vacuole.Molecular biology of the cell · 2026Article
- Subcellular Cartography of the Phosphoinositide Multiverse.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2026Review
- Differential effects of lysophospholipid headgroups, acyl chain length and saturation on vacuole acidification, CaFrontiers in cell and developmental biology · 2026Article
- Lysosomal swelling triggers LRRK2 activity.bioRxiv : the preprint server for biology · 2025Article
- Lysosome heterogeneity and diversity mapped through its distinct cellular functions.Cellular and molecular life sciences : CMLS · 2025Review
- ATG16L1 controls mammalian vacuolar proton ATPase.The Journal of cell biology · 2025Article
- Mechanism of phosphoinositide regulation of lysosomal pH via inhibition of CLC-7.bioRxiv : the preprint server for biology · 2025Article
- Control of Golgi- V-ATPase through Sac1-dependent co-regulation of PI(4)P and cholesterol.Nature communications · 2025Article
- An advanced toolset to manipulate and monitor subcellular phosphatidylinositol 3,5-bisphosphate.The Journal of cell biology · 2025Article
- PIPNature communications · 2025Article
- Regulatory dynamics of Sch9 in response to cytosolic acidification: From spatial reconfiguration to cellular adaptation to stresses.iScience · 2025Article
- PI(3,5)P2 asymmetry during mitosis is essential for asymmetric vacuolar inheritance.The Journal of cell biology · 2025Article
- Yeast TLDc domain proteins regulate assembly state and subcellular localization of the V-ATPase.The EMBO journal · 2024Article
- Phospholipids Differentially Regulate CaACS chemical biology · 2024Article
- Mining key circRNA-associated-ceRNA networks for milk fat metabolism in cows with varying milk fat percentages.BMC genomics · 2024Article
- DEAD-Box RNA Helicase Family in Physic Nut (Plants (Basel, Switzerland) · 2024Article
- The Human Mutation K237_V238del in a Putative Lipid Binding Motif within the V-ATPase a2 Isoform Suggests a Molecular Mechanism Underlying Cutis Laxa.International journal of molecular sciences · 2024Article
29 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Vacuolar proton-translocating ATPases (V-ATPases) are highly conserved, ATP-driven proton pumps regulated by reversible dissociation of its cytosolic, peripheral V1 domain from the integral membrane V(o) domain. Multiple stresses induce changes in V1-V(o) assembly, but the signaling mechanisms behind these changes are not understood. Here we show that certain stress-responsive changes in V-ATPase activity and assembly require the signaling lipid phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2). V-ATPase activation through V1-V(o) assembly in response to salt stress is strongly dependent on PI(3,5)P2 synthesis. Purified V(o) complexes preferentially bind to PI(3,5)P2 on lipid arrays, suggesting direct binding between the lipid and the membrane sector of the V-ATPase. Increasing PI(3,5)P2 levels in vivo recruits the N-terminal domain of V(o)-sector subunit Vph1p from cytosol to membranes, independent of other subunits. This Vph1p domain is critical for V1-V(o) interaction, suggesting that interaction of Vph1p with PI(3,5)P2-containing membranes stabilizes V1-V(o) assembly and thus increases V-ATPase activity. These results help explain the previously described vacuolar acidification defect in yeast fab1 and vac14 mutants and suggest that human disease phenotypes associated with PI(3,5)P2 loss may arise from compromised V-ATPase stability and regulation.
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