ArticlePLoS biology2014
A conserved endoplasmic reticulum membrane protein complex (EMC) facilitates phospholipid transfer from the ER to mitochondria.
Article in PLoS biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers, 1 of them a synthesis that pooled it.
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Who cites it
186 citing papers in PubMed, 1 synthesis or guideline pooled it, 302 citations in OpenAlex.
- Inter-organellar Communication in Parkinson's and Alzheimer's Disease: Looking Beyond Endoplasmic Reticulum-Mitochondria Contact Sites.Frontiers in neuroscience · 2022Pooled it
- Short-term oral pre-exposure prophylaxis against HIV-1 modulates the transcriptome of foreskin tissue in young men in Africa.Frontiers in immunology · 2022Trial
- Mitochondrial membrane remodeling in stress adaptation: Lipid control of organelle quality.Protein science : a publication of the Protein Society · 2026Review
- Rewiring mitochondrial phosphatidylethanolamine metabolism identifies new and unaccounted trafficking steps.Journal of lipid research · 2026Article
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Advancing the monitoring of organelle contact sites in vitro and in vivo.Biochemical Society transactions · 2026Review
- Membrane Protein Folding and Biogenesis: Insights from Single-Molecule Force Spectroscopy.Chemical reviews · 2026Review
- Rewiring Mitochondrial Phosphatidylethanolamine Metabolism Identifies New and Unaccounted Trafficking Steps.bioRxiv : the preprint server for biology · 2026Article
- Article
- A guide to characterizing the dynamic mitochondria-endoplasmic reticulum contact sites.The FEBS journal · 2025Review
- Cvm1 and its paralogue Cvm2 function as a complex at vacuolar membrane contact sites.Molecular biology of the cell · 2025Article
- The Vps13-like protein BLTP2 regulates phosphatidylethanolamine levels to maintain plasma membrane fluidity and breast cancer aggressiveness.Nature cell biology · 2025Article
- Ltc1 localization by EMC regulates cell membrane fluidity to facilitate membrane protein biogenesis.iScience · 2025Article
- The Endoplasmic Reticulum Membrane Protein Complex Is Important for Deoxynivalenol Production and the Virulence ofJournal of fungi (Basel, Switzerland) · 2025Article
- Comparative 3D ultrastructure of Plasmodium falciparum gametocytes.Nature communications · 2025Article
- EMC3 is critical for CFTR function and calcium mobilization in the mouse intestinal epithelium.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- CLSTN3B promotes lipid droplet maturation and lipid storage in mouse adipocytes.Nature communications · 2024Article
- Imaging interorganelle contacts at a glance.Journal of cell science · 2024Review
- EMC1 Is Required for the Sarcoplasmic Reticulum and Mitochondrial Functions in theBiomolecules · 2024Article
- A promising anti-tumor targeting on ERMMDs mediated abnormal lipid metabolism in tumor cells.Cell death & disease · 2024Review
126 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitochondrial membrane biogenesis and lipid metabolism require phospholipid transfer from the endoplasmic reticulum (ER) to mitochondria. Transfer is thought to occur at regions of close contact of these organelles and to be nonvesicular, but the mechanism is not known. Here we used a novel genetic screen in S. cerevisiae to identify mutants with defects in lipid exchange between the ER and mitochondria. We show that a strain missing multiple components of the conserved ER membrane protein complex (EMC) has decreased phosphatidylserine (PS) transfer from the ER to mitochondria. Mitochondria from this strain have significantly reduced levels of PS and its derivative phosphatidylethanolamine (PE). Cells lacking EMC proteins and the ER-mitochondria tethering complex called ERMES (the ER-mitochondria encounter structure) are inviable, suggesting that the EMC also functions as a tether. These defects are corrected by expression of an engineered ER-mitochondrial tethering protein that artificially tethers the ER to mitochondria. EMC mutants have a significant reduction in the amount of ER tethered to mitochondria even though ERMES remained intact in these mutants, suggesting that the EMC performs an additional tethering function to ERMES. We find that all Emc proteins interact with the mitochondrial translocase of the outer membrane (TOM) complex protein Tom5 and this interaction is important for PS transfer and cell growth, suggesting that the EMC forms a tether by associating with the TOM complex. Together, our findings support that the EMC tethers ER to mitochondria, which is required for phospholipid synthesis and cell growth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.