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Drp1-dependent mitochondrial fission via MiD49/51 is essential for apoptotic cristae remodeling

Hidenori Otera1, Non Miyata2, Osamu Kuge2

  • 1Graduate School of Medical Sciences, Kyushu University, Fukuoka 819-0395, Japan.

The Journal of Cell Biology
|February 24, 2016
PubMed

Insights

Mitochondrial fission

Area of Science:

  • Cell Biology
  • Biochemistry

Background:

  • Mitochondrial fission is crucial for intrinsic apoptosis, involving Drp1 and its receptors Mff, MiD49, and MiD51.
  • The precise roles of these receptors in fission-mediated cytochrome c release remain unclear.

Purpose of the Study:

  • To elucidate the functional roles of mitochondrial fission receptors (Mff, MiD49, MiD51) in intrinsic apoptosis.
  • To investigate the mechanism by which Drp1-mediated fission facilitates cytochrome c release.

Main Methods:

  • Utilized knockout (KO) cell lines for Mff, MiD49/MiD51, and Drp1.
  • Assessed cristae remodeling and cytochrome c release during apoptosis.
  • Investigated the impact of OPA1 depletion and OPA1 oligomer disassembly.

Main Results:

  • MiD49/MiD51-KO and Drp1-KO cells resisted cristae remodeling and cytochrome c release.
  • The phenotype in MiD49/51-KO cells was abolished by OPA1 depletion, unlike in Drp1-KO cells.
  • OPA1 oligomer disassembly occurred similarly in Drp1-KO and MiD49/51-KO cells, unlinked to cristae remodeling.

Conclusions:

  • Drp1-dependent mitochondrial fission, mediated by MiD49/MiD51, is essential for cristae remodeling during intrinsic apoptosis.
  • OPA1 oligomer disassembly is not the direct cause of cristae remodeling for cytochrome c release.

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