ArticleiScience2022
Dissociation of ERMES clusters plays a key role in attenuating the endoplasmic reticulum stress.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Genomic signatures of host-range divergence in the generalist Beauveria bassiana and the specialist Beauveria brongniartii.Molecular genetics and genomics : MGG · 2026Article
- Mitochondria in the middle of inter- organellar cross talk: insights from yeast to humans.Frontiers in cell and developmental biology · 2026Review
- MyD88 polymerization and association to cellular membranes in a yeast heterologous model.Cellular and molecular life sciences : CMLS · 2025Article
- Mitochondria-plasma membrane contact sites regulate the ER-mitochondria encounter structure.Journal of cell science · 2025Article
- Dnm1 Is Required for the Focal Clustering of Fis1 on the Mitochondrial Outer Membrane.microPublication biology · 2025Article
- Chemical inhibition of phosphatidylcholine biogenesis reveals its role in mitochondrial division.iScience · 2024Article
- Navigating the landscape of mitochondrial-ER communication in health and disease.Frontiers in molecular biosciences · 2024Review
- Genetically Encoded Tools to Monitor and Interrogate Membrane Contact Sites.Contact (Thousand Oaks (Ventura County, Calif.))Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In yeast, ERMES, which mediates phospholipid transport between the ER and mitochondria, forms a limited number of oligomeric clusters at ER-mitochondria contact sites in a cell. Although the number of the ERMES clusters appears to be regulated to maintain proper inter-organelle phospholipid trafficking, its underlying mechanism and physiological relevance remain poorly understood. Here, we show that mitochondrial dynamics control the number of ERMES clusters. Moreover, we find that ER stress causes dissociation of the ERMES clusters independently of Ire1 and Hac1, canonical ER-stress response pathway components, leading to a delay in the phospholipid transport from the ER to mitochondria. Our biochemical and genetic analyses strongly suggest that the impaired phospholipid transport contributes to phospholipid accumulation in the ER, expanding the ER for ER stress attenuation. We thus propose that the ERMES dissociation constitutes an overlooked pathway of the ER stress response that operates in addition to the canonical Ire1/Hac1-dependent pathway.
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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.