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ER-associated mitochondrial division links the distribution of mitochondria and mitochondrial DNA in yeast
Open accessAbstract
Mitochondrial division is important for mitochondrial distribution and function. Recent data have demonstrated that ER-mitochondria contacts mark mitochondrial division sites, but the molecular basis and functions of these contacts are not understood. Here we show that in yeast, the ER-mitochondria tethering complex, ERMES, and the highly conserved Miro GTPase, Gem1, are spatially and functionally linked to ER-associated mitochondrial division. Gem1 acts as a negative regulator of ER-mitochondria contacts, an activity required for the spatial resolution and distribution of newly generated mitochondrial tips following division. Previous data have demonstrated that ERMES localizes with a subset of actively replicating mitochondrial nucleoids. We show that mitochondrial division is spatially linked to nucleoids and that a majority of these nucleoids segregate prior to division, resulting in their distribution into newly generated tips in the mitochondrial network. Thus, we postulate that ER-associated division serves to link the distribution of mitochondria and mitochondrial nucleoids in cells. DOI:http://dx.doi.org/10.7554/eLife.00422.001.
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“At the fission site of mitochondria, the ERMES complex localizes adjacent to replicating mtDNA and is involved in the distribution of newly replicated mtDNA to the dividing mitochondria [33].”
From In Candida glabrata, ERMES Component GEM1 Controls Mitochondrial Morphology, mtROS, and Drug Efflux Pump Expression, Resulting in Azole Susceptibility (2023) · cites this paper as [33]
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In the citing paper
“After mitochondrial fission, one of the dividing mitochondria is detached from the ER, a process that requires Gem1 in S. cerevisiae [33].”
From In Candida glabrata, ERMES Component GEM1 Controls Mitochondrial Morphology, mtROS, and Drug Efflux Pump Expression, Resulting in Azole Susceptibility (2023) · cites this paper as [33]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In S. cerevisiae, mutations leading to decreased GTPase activity, Gem1(S19N) or Gem1(S462N), impair the maintenance of mitochondrial morphology and dissociation of ERMES from the fission site [33].”
From In Candida glabrata, ERMES Component GEM1 Controls Mitochondrial Morphology, mtROS, and Drug Efflux Pump Expression, Resulting in Azole Susceptibility (2023) · cites this paper as [33]
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“The fission site of mitochondria is wrapped around by ER tubules [44], where the ERMES complex localizes [33].”
From In Candida glabrata, ERMES Component GEM1 Controls Mitochondrial Morphology, mtROS, and Drug Efflux Pump Expression, Resulting in Azole Susceptibility (2023) · cites this paper as [33]
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“As the ERMES plays an important role in mitochondrial fission [33], the impact of each subunit on azole resistance was evaluated.”
From In Candida glabrata, ERMES Component GEM1 Controls Mitochondrial Morphology, mtROS, and Drug Efflux Pump Expression, Resulting in Azole Susceptibility (2023) · cites this paper as [33]
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“The detection of ERMES foci by fluorescence imaging may underestimate ERMES foci associated with mitochondrial division as we observed a positive correlation between the percentage of mitochondrial divisions associated with a given ERMES subunit and its estimated whole-cell abundance (Huh et al., 2003).”
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Self-citationPINK1 and Parkin Target Miro for Phosphorylation and Degradation to Arrest Mitochondrial Motility
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Metadata
- Authors
- Murley, A., Lackner, L. L., Osman, C., West, M., Voeltz, G. K., Walter, P., & Nunnari, J.
- Affiliations
- University of California, Davis (US)
- University of California, San Francisco (US)
- University of Colorado Boulder (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Nunnari, Jodi
- Venue
- eLife
- Publisher
- eLife Sciences Publications, Ltd
- Published
- 2013-05-14
- Volume
- 2
- Pages
- e00422-e00422
- ISSN
- 2050-084X (ISSN-L)
- PMC
- PMC3654481
- OpenAlex
- W2130893307
- Cited by
- 326
- References
- 55
- Citations by year
- 2026: 7 · 2025: 20 · 2024: 17 · 2023: 16 · 2022: 19 · 2021: 26 · 2020: 34 · 2019: 27 · 2018: 32 · 2017: 26 · 2016: 29 · 2015: 28 · 2014: 31 · 2013: 14
- FWCI
- 15.24
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- eLife (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (5T32GM007377-34, R01GM097432, RO1GM083977)
- Howard Hughes Medical Institute
- Human Frontier Science Program
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Keywords
- mitochondrial division, ER-mitochondria contact sites, ERMES, mitochondrial nucleoids, mitochondrial DNA segregation, mitochondrial distribution, yeast
- MeSH terms
- DNA, Fungal, DNA, Mitochondrial, Endoplasmic Reticulum, Mitochondria, Saccharomyces cerevisiae, Signal Transduction, Saccharomyces cerevisiae Proteins, Multiprotein Complexes, Mitochondrial Dynamics
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