ArticleNature communications2021
Emr1 regulates the number of foci of the endoplasmic reticulum-mitochondria encounter structure complex.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 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
- Mitochondrial Genetic Diseases and Ophthalmic Manifestations: Molecular Pathophysiology, Genetics, and Clinical Management.International journal of molecular sciences · 2026Review
- Mitochondria-plasma membrane contact sites regulate the ER-mitochondria encounter structure.Journal of cell science · 2025Article
- Molecular Mechanisms of Pathogenic Fungal Virulence Regulation by Cell Membrane Phospholipids.Journal of fungi (Basel, Switzerland) · 2025Review
- Ltc1 localization by EMC regulates cell membrane fluidity to facilitate membrane protein biogenesis.iScience · 2025Article
- Endoplasmic reticulum-mitochondria crosstalk: new mechanisms in the development of atherosclerosis.Frontiers in endocrinology · 2025Review
- Biogenesis of mitochondrial β-barrel membrane proteins.FEBS open bio · 2024Review
- The Mitochondrial Distribution and Morphology Family 33 GeneJournal of fungi (Basel, Switzerland) · 2024Article
- The divergent ER-mitochondria encounter structures (ERMES) are conserved in parabasalids but lost in several anaerobic lineages with hydrogenosomes.BMC biology · 2023Article
- Article
- Fission yeast cells mix parental mitochondria in a progressive manner during meiosis.Journal of molecular cell biology · 2023Article
- Microtubule-mitochondrial attachment facilitates cell division symmetry and mitochondrial partitioning in fission yeast.Journal of cell science · 2023Article
- Dissociation of ERMES clusters plays a key role in attenuating the endoplasmic reticulum stress.iScience · 2022Article
- TraB family proteins are components of ER-mitochondrial contact sites and regulate ER-mitochondrial interactions and mitophagy.Nature communications · 2022Article
- Multilocation proteins in organelle communication: Based on protein-protein interactions.Plant direct · 2022Article
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Identification of key differential genes in intimal hyperplasia induced by left carotid artery ligation.PeerJ · 2022Article
- HIV infection of astrocytes compromises inter-organelle interactions and inositol phosphate metabolism: A potential mechanism of bystander damage and viral reservoir survival.Progress in neurobiology · 2021Article
- Mechanisms of Non-Vesicular Exchange of Lipids at Membrane Contact Sites: Of Shuttles, Tunnels and, Funnels.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endoplasmic reticulum-mitochondria encounter structure (ERMES) complex creates contact sites between the endoplasmic reticulum and mitochondria, playing crucial roles in interorganelle communication, mitochondrial fission, mtDNA inheritance, lipid transfer, and autophagy. The mechanism regulating the number of ERMES foci within the cell remains unclear. Here, we demonstrate that the mitochondrial membrane protein Emr1 contributes to regulating the number of ERMES foci. We show that the absence of Emr1 significantly decreases the number of ERMES foci. Moreover, we find that Emr1 interacts with the ERMES core component Mdm12 and colocalizes with Mdm12 on mitochondria. Similar to ERMES mutant cells, cells lacking Emr1 display defective mitochondrial morphology and impaired mitochondrial segregation, which can be rescued by an artificial tether capable of linking the endoplasmic reticulum and mitochondria. We further demonstrate that the cytoplasmic region of Emr1 is required for regulating the number of ERMES foci. This work thus reveals a crucial regulatory protein necessary for ERMES functions and provides mechanistic insights into understanding the dynamic regulation of endoplasmic reticulum-mitochondria communication.
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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.