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C3orf33/MISO regulates mitochondrial homeostasis via mitophagy
Jianshuang Li1,2,3, Wenjun Wang3, Li He4
1The Department of Orthopaedics, Guangzhou Red Cross Hospital, Faculty of Medical Science, Jinan University, Guangzhou, China.
Autophagy
|January 22, 2026
Summary
Researchers discovered C3orf33/MISO protein regulates mitochondrial stress response. This protein forms specialized subdomains (SMEM) to clear damaged mitochondrial DNA (mtDNA) via mitophagy, maintaining cellular health.
Area of Science:
- Cell Biology
- Mitochondrial Biology
- Molecular Biology
Background:
- Mitochondria maintain cellular homeostasis through dynamic remodeling and stress-response pathways.
- Peripheral mitochondrial fission forms small, MTFP1-enriched mitochondria (SMEM) that sequester damaged mitochondrial DNA (mtDNA) for autophagic degradation.
- The mechanisms governing SMEM biogenesis are not fully understood.
Purpose of the Study:
- To identify and characterize the protein responsible for regulating stress-induced mitochondrial subdomain formation.
- To elucidate the molecular mechanism by which SMEM biogenesis is controlled.
- To understand the role of SMEM in maintaining mitochondrial homeostasis under stress.
Main Methods:
- Utilized *Drosophila* and mammalian cell culture models.
- Investigated protein localization and interactions using immunofluorescence and biochemical assays.
- Analyzed mitochondrial dynamics, fission, and fusion events.
- Assessed the impact of C3orf33/MISO on mtDNA integrity and mitophagy.
Main Results:
- Identified C3orf33/MISO as a conserved regulator of mitochondrial dynamics and stress-induced subdomain formation.
- C3orf33/MISO is an inner mitochondrial membrane protein that promotes fission by recruiting MTFP1 and suppresses fusion by excluding OPA1.
- Upon stress, C3orf33/MISO stabilizes, initiating SMEM assembly that targets damaged mtDNA for clearance via mitophagy.
Conclusions:
- C3orf33/MISO is a key regulator of SMEM biogenesis, essential for mitochondrial stress response.
- SMEM compartments act as hubs for IMM reorganization and mtDNA quality control.
- The C3orf33/MISO-mediated pathway is critical for preserving mitochondrial homeostasis under stress.
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