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Related Experiment Videos

Splitting the apoptosome.

Andrew T Ho1, Eldad Zacksenhaus

  • 1Division of Cell & Molecular Biology, Toronto General Research Institute-University Health Network, Toronto, Ontario, Canada.

Cell Cycle (Georgetown, Tex.)
|March 17, 2004
PubMed
Summary
This summary is machine-generated.

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Mitochondrial permeabilization triggers apoptosome assembly, activating caspase-9. However, new evidence shows caspase-9 can be activated independently of the mitochondria and Apaf1 in certain cells, revealing alternative apoptotic pathways.

Area of Science:

  • Cellular biology
  • Biochemistry
  • Apoptosis research

Background:

  • The intrinsic apoptotic pathway typically involves mitochondrial permeabilization and apoptosome assembly.
  • Apoptosome formation requires cytochrome c binding to Apaf1, leading to pro-caspase-9 activation.

Purpose of the Study:

  • To investigate alternative pathways for caspase-9 activation.
  • To determine if caspase-9 can be activated independently of the apoptosome and mitochondria.

Main Methods:

  • Studied caspase-9 activation in Apaf1-mutant primary myoblasts and fibroblasts.
  • Utilized stimuli known to induce mitochondrial-dependent apoptosis.

Main Results:

  • Caspase-9 activation was observed in Apaf1-mutant primary myoblasts, but not fibroblasts.

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  • This activation occurred in response to stimuli typically acting via mitochondria.
  • Suggests tissue-specific, context-dependent pathways for caspase-9 activation exist.

    • Conclusions:

    • Apoptosomal activation of caspase-9 is not the sole route.
    • Alternative pathways can bypass Apaf1 and mitochondria for caspase-9 activation.
    • These alternative pathways are tissue and context specific.