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Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9

K Kuida1, T F Haydar, C Y Kuan

  • 1Vertex Pharmaceuticals Incorporated, Cambridge, Massachusetts 02139, USA.

Cell
|August 26, 1998
PubMed

Insights

Caspase 9 (Casp9) is crucial for initiating the cell death cascade. Gene targeting in mice revealed Casp9 is essential for apoptosis during brain development and caspase activation.

Area of Science:

  • Cellular biology
  • Developmental biology
  • Molecular genetics

Background:

  • Caspases are key executioners of programmed cell death (apoptosis) in mammals.
  • The precise upstream activators initiating the caspase cascade remain incompletely understood.
  • Caspase 9 (Casp9) is a candidate initiator caspase.

Purpose of the Study:

  • To investigate the role of Caspase 9 (Casp9) as an upstream activator of the caspase cascade.
  • To determine the in vivo function of Casp9 in mammalian apoptosis.

Main Methods:

  • Gene targeting in mice to create Casp9 knockout models.
  • Analysis of embryonic brain development and apoptosis in Casp9-deficient mice.
  • Assessment of caspase activation and cleavage in thymocytes and cell extracts.

Main Results:

  • Casp9 knockout mice exhibit perinatal lethality with severe brain malformations due to reduced apoptosis.
  • Casp9 deletion prevents Caspase 3 (Casp3) activation in embryonic brains.
  • Casp9-deficient cells show resistance to apoptosis, lacking Casp3-like cleavage and DNA fragmentation.

Conclusions:

  • Caspase 9 (Casp9) is a critical upstream activator of the caspase cascade in vivo.
  • Casp9 plays an essential role in regulating apoptosis during mammalian brain development.

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