Drp1-dependent mitochondrial fission via MiD49/51 is essential for apoptotic cristae remodeling
Open accessAbstract
Mitochondrial fission facilitates cytochrome c release from the intracristae space into the cytoplasm during intrinsic apoptosis, although how the mitochondrial fission factor Drp1 and its mitochondrial receptors Mff, MiD49, and MiD51 are involved in this reaction remains elusive. Here, we analyzed the functional division of these receptors with their knockout (KO) cell lines. In marked contrast to Mff-KO cells, MiD49/MiD51-KO and Drp1-KO cells completely resisted cristae remodeling and cytochrome c release during apoptosis. This phenotype in MiD49/51-KO cells, but not Drp1-KO cells, was completely abolished by treatments disrupting cristae structure such as OPA1 depletion. Unexpectedly, OPA1 oligomers generally thought to resist cytochrome c release by stabilizing the cristae structure were similarly disassembled in Drp1-KO and MiD49/51-KO cells, indicating that disassembly of OPA1 oligomers is not directly linked to cristae remodeling for cytochrome c release. Together, these results indicate that Drp1-dependent mitochondrial fission through MiD49/MiD51 regulates cristae remodeling during intrinsic apoptosis.
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The release of CYCS and SMAC to the cytosol is favored by mitochondrial cristae remodeling, which relies on the oligomerization and activation of OPA1, possibly preceded by BAX-dependent and BAK-dependent activation of OMA1 and/or DRP1.
“The release of CYCS and SMAC to the cytosol is favored by mitochondrial cristae remodeling [164], which relies on the oligomerization and activation of OPA1, mitochondrial dynamin like GTPase (OPA1) [165], possibly preceded by the BAX-dependent and BAK-dependent activation of OMA1 zinc metallopeptidase (OMA1) [166, 167], and/or dynamin 1 like (DNM1L; best known as DRP1) [168].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [168]
DRP1-dependent mitochondrial fission through MiD49 and/or MiD51, but not MFF, is required for cristae remodeling to facilitate cytochrome c release into the cytoplasm during apoptosis.
“DRP1-dependent mitochondrial fission through MiD49 and/or MiD51, but not MFF, is required for cristae remodeling to facilitate cytochrome c release into the cytoplasm during apoptosis [97].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [97]
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References 46 · Cited by 229
- Authors
- Otera, H., Miyata, N., Kuge, O., & Mihara, K.
- Affiliations
- Kyushu University (JP)
- Corresponding author
- Mihara, Katsuyoshi
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2016-02-22
- Volume
- 212
- Issue
- 5
- Pages
- 531-544
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC4772499
- OpenAlex
- W2278561515
- Cited by
- 229
- References
- 46
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 17 · 2023: 23 · 2022: 36 · 2021: 24 · 2020: 23 · 2019: 27 · 2018: 15 · 2017: 29 · 2016: 12
- FWCI
- 14.37
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science, and Technology (25440088, 25291046, 22370071, 24657138)
- Takeda Science Foundation
- Inamori Foundation
- Uehara Memorial Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial fission, Drp1, MiD51, Mff, mitochondrial apoptosis, cytochrome c release, mitochondrial membrane structure, mitochondrial receptors
- MeSH terms
- Cytoplasm, HeLa Cells, Humans, Microtubule-Associated Proteins, Mitochondria, Peptide Elongation Factors, Tumor Cells, Cultured, Apoptosis, GTP Phosphohydrolases, Mitochondrial Proteins, Dynamins, Cytochromes c
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