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Abstract
MTFR1L is identified as a critical component in coordinating mitochondrial fission with mitophagy initiation.
- MTFR1L is enriched at sites where the ULK1 kinase is localized, indicating its role in mitophagy initiation.
- Depletion of MTFR1L leads to decreased respiratory capacity, increased apoptosis, and impaired mitophagy flux.
- MTFR1L undergoes phosphorylation dependent on ULK1 kinase during mitophagy induction, suggesting a regulatory role.
- MTFR1L is necessary for the stability of ATG13, linking it to the autophagy process.
- The findings suggest a feedback loop between MTFR1L and ULK1 that may influence cell survival.
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