ArticleProceedings of the National Academy of Sciences of the United States of America2022
Spns1 is a lysophospholipid transporter mediating lysosomal phospholipid salvage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 61 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- MFSD2A in health and disease: lysolipid transport, barrier physiology, and translational boundaries.Molecular biomedicine · 2026Review
- The lipidomic atlas for cellular organelles to reveal the central role of mitochondria in organelle communication.Science China. Life sciences · 2026Article
- Structure and mechanism of human sphingosine-1-phosphate transporter MFSD2B.Nature communications · 2026Article
- Proton-coupled alternating access in a versatile mycobacterial Spns drug transporter.Research square · 2026Article
- SLC26A11 is an atypical solute carrier with dual transport-channel function mediating lysosomal sulfate transport.Nature communications · 2026Article
- Proton-coupled alternating access in a versatile mycobacterial Spns drug transporter.bioRxiv : the preprint server for biology · 2026Article
- Peroxisome-derived ether lipids regulate lysosomal exocytosis.The EMBO journal · 2026Article
- LPLAT7 reutilizes unsaturated 1-lysophospholipids formed during lysosomal phospholipid degradation.Journal of lipid research · 2026Article
- Structure and mechanism of human sphingosine-1-phosphate transporter MFSD2B.bioRxiv : the preprint server for biology · 2026Article
- SPNS1 is an essential cellular factor for EV-A71 by acting as a transporter of viral pocket factor.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Enzyme Activity-Based Genome-wide Screening for Modifiers of Lysosomal Glucocerebrosidase Uncovers Candidate Risk Factors for Parkinson's Disease.ACS central science · 2025Article
- Proteomic profiling identifies miR-423-5p as a modulator of oncogenic metabolism in HCC.Journal of translational medicine · 2025Article
- SPNS1 variants cause multiorgan disease and implicate lysophospholipid transport as critical for mTOR-regulated lipid homeostasis.The Journal of clinical investigation · 2025Article
- MFSD2A in Focus: the Molecular Mechanism of Omega-3 Fatty Acid Transport.Physiology (Bethesda, Md.) · 2025Review
- Targeting phospholipase PLAG-15 promotes healthy aging iniScience · 2025Article
- Quantitative modeling of rod outer segment phagocytosis and recycling.Scientific reports · 2025Article
- Broken Balance: Emerging Cross-Talk Between Proteostasis and Lipostasis in Neurodegenerative Diseases.Cells · 2025Review
- Transport and inhibition of the sphingosine-1-phosphate exporter SPNS2.Nature communications · 2025Article
- Molecular basis of Spns1-mediated lysophospholipid transport from the lysosome.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
The lysosome is central to the degradation of proteins, carbohydrates, and lipids and their salvage back to the cytosol for reutilization. Lysosomal transporters for amino acids, sugars, and cholesterol have been identified, and the metabolic fates of these molecules in the cytoplasm have been elucidated. Remarkably, it is not known whether lysosomal salvage exists for glycerophospholipids, the major constituents of cellular membranes. By using a transport assay screen against orphan lysosomal transporters, we identified the major facilitator superfamily protein Spns1 that is ubiquitously expressed in all tissues as a proton-dependent lysophosphatidylcholine (LPC) and lysophosphatidylethanolamine (LPE) transporter, with LPC and LPE being the lysosomal breakdown products of the most abundant eukaryotic phospholipids, phosphatidylcholine and phosphatidylethanolamine, respectively. Spns1 deficiency in cells, zebrafish embryos, and mouse liver resulted in lysosomal accumulation of LPC and LPE species with pathological consequences on lysosomal function. Flux analysis using stable isotope-labeled phospholipid apolipoprotein E nanodiscs targeted to lysosomes showed that LPC was transported out of lysosomes in an Spns1-dependent manner and re-esterified back into the cytoplasmic pools of phosphatidylcholine. Our findings identify a phospholipid salvage pathway from lysosomes to the cytosol that is dependent on Spns1 and critical for maintaining normal lysosomal function.
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