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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
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Published on: February 16, 2015

Resistance to caspase-independent cell death requires persistence of intact mitochondria

Stephen W G Tait1, Melissa J Parsons, Fabien Llambi

  • 1Department of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.

Developmental Cell
|May 25, 2010
PubMed

Insights

Mitochondria can resist outer membrane permeabilization (MOMP) during apoptosis, enabling cell recovery. This incomplete MOMP (iMOMP) provides a source of intact mitochondria crucial for survival when caspases are inhibited.

Area of Science:

  • Cell biology
  • Molecular biology
  • Biochemistry

Background:

  • Mitochondrial outer membrane permeabilization (MOMP) is a critical step in apoptosis.
  • Caspase-independent cell death pathways exist, but resistance mechanisms are not fully understood.
  • Mitochondrial recovery is implicated in cellular survival following apoptotic stimuli.

Purpose of the Study:

  • To investigate the phenomenon of resistance to MOMP-dependent cell death.
  • To identify the role of intact mitochondria in cellular recovery after MOMP.
  • To explore the mechanisms underlying resistance to MOMP.

Main Methods:

  • Live cell imaging to observe mitochondrial dynamics during apoptosis.
  • Utilized various apoptotic stimuli and cell types.
  • Employing Bcl-2 antagonist ABT-737 to probe Bax/Bak activation.

Main Results:

  • Observed incomplete MOMP (iMOMP) where not all mitochondria undergo permeabilization.
  • iMOMP occurs across different cell types and stimuli, irrespective of caspase activity.
  • The presence of intact mitochondria correlated with cellular recovery, especially when caspases were blocked.
  • Resistance to MOMP appears to be at the level of Bax or Bak activation.

Conclusions:

  • Incomplete MOMP (iMOMP) is a significant biological process.
  • iMOMP generates a pool of intact mitochondria essential for cell survival.
  • This provides a mechanism for resistance to MOMP-dependent, caspase-independent cell death.

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