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Orthogonal Targeting of SAC1 to Mitochondria Implicates ORP2 as a Major Player in PM PI4P Turnover.
Article in Contact (Thousand Oaks (Ventura County, Calif.)). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 8 citations in OpenAlex.
- Quantitative comparison of PI(3,5)PMolecular biology of the cell · 2026Article
- Endogenous tracking reveals paralog-specific targets for phosphatidic acid generation during phospholipase C signaling in living cells.The Journal of biological chemistry · 2026Article
- Article
- Disruption of the PIKfyve complex unveils an adaptive mechanism to promote lysosomal repair and mitochondrial homeostasis.Nature communications · 2025Article
- Quantitative comparison of PI(3,5)PbioRxiv : the preprint server for biology · 2025Article
- PILS-Nir1 is a sensitive phosphatidic acid biosensor that reveals mechanisms of lipid production.The Journal of cell biology · 2025Article
- PILS-Nir1 is a novel phosphatidic acid biosensor that reveals mechanisms of lipid production.bioRxiv : the preprint server for biology · 2025Article
- Mitochondria-ER-PM contacts regulate mitochondrial division and PI(4)P distribution.The Journal of cell biology · 2024Article
- OSBP is a major determinant of Golgi phosphatidylinositol 4-phosphate homeostasis.bioRxiv : the preprint server for biology · 2024Article
- Editorial on Special Collection inContact (Thousand Oaks (Ventura County, Calif.))Article
- OSBP is a Major Determinant of Golgi Phosphatidylinositol 4-Phosphate Homeostasis.Contact (Thousand Oaks (Ventura County, Calif.))Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Oxysterol-binding protein (OSBP)-related proteins (ORPs) 5 and 8 have been shown to deplete the lipid phosphatidylinositol 4-phosphate (PI4P) at sites of membrane contact between the endoplasmic reticulum (ER) and plasma membrane (PM). This is believed to be caused by transport of PI4P from the PM to the ER, where PI4P is degraded by an ER-localized SAC1 phosphatase. This is proposed to power the anti-port of phosphatidylserine (PS) lipids from ER to PM, up their concentration gradient. Alternatively, ORPs have been proposed to sequester PI4P, dependent on the concentration of their alternative lipid ligand. Here, we aimed to distinguish these possibilities in living cells by orthogonal targeting of PI4P transfer and degradation to PM-mitochondria contact sites. Surprisingly, we found that orthogonal targeting of SAC1 to mitochondria enhanced PM PI4P turnover independent of targeting to contact sites with the PM. This turnover could be slowed by knock-down of soluble ORP2, which also has a major impact on PM PI4P levels even without SAC1 over-expression. The data reveal a role for contact site-independent modulation of PM PI4P levels and lipid antiport.
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