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Pre-processed caspase-9 contained in mitochondria participates in apoptosis

P Costantini1, J-M Bruey, M Castedo

  • 1Centre National de la Recherche Scientifique, UMR1599, Institut Gustave Roussy, 39 rue Camille-Desmoulins, F-94805 Villejuif, France.

Insights

Mitochondria contain pre-processed caspase-9 in non-apoptotic cells, a finding observed across various organs. This mitochondrial caspase-9 is released upon cell permeability changes, impacting apoptosis regulation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Mitochondria play a crucial role in apoptosis.
  • Caspase-9 is a key initiator caspase in the intrinsic apoptosis pathway.
  • The localization and processing of caspase-9 are critical for its function.

Purpose of the Study:

  • To investigate the presence and processing state of caspase-9 within mitochondria.
  • To determine the cellular localization of caspase-9 in different cell types and under various conditions.
  • To elucidate the role of Bcl-2 in regulating mitochondrial caspase-9 activity.

Main Methods:

  • Mitochondrial purification from various organs (liver, brain, kidney, spleen, heart).
  • Induction of mitochondrial permeability transition in vitro.
  • Subcellular fractionation and immunofluorescence assays.
  • Western blotting using antibodies specific for pro-caspase-9 and processed caspase-9.

Main Results:

  • Mitochondria from diverse organs contain both pro-caspase-9 and mature caspase-9.
  • Liver mitochondria release mature caspase-9 upon induction of permeability transition.
  • SHEP neuroblastoma cells constitutively harbor pre-processed caspase-9 in mitochondria, unlike HeLa cells.
  • Apoptosis induction causes mitochondrial pro-caspase-9 translocation to cytosol/nucleus, an event inhibited by Bcl-2.

Conclusions:

  • Mitochondria can store pre-processed caspase-9 in non-apoptotic cells.
  • Bcl-2 regulates apoptosis by preventing mitochondrial caspase-9 interaction with cytosolic activators via membrane permeabilization control.
  • This finding reveals a novel mechanism for apoptosis regulation involving mitochondrial caspase localization and processing.

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