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Bak and Bax are non-redundant during infection- and DNA damage-induced apoptosis

Oliver Kepp1, Krishnaraj Rajalingam, Sonja Kimmig

  • 1Department of Molecular Biology, Max Planck Institute for Infection Biology, Research Group for Molecular Infection and Tumor Biology, Berlin, Germany.

The EMBO Journal
|January 20, 2007
PubMed

Insights

Bak and Bax are crucial for Neisseria gonorrhoeae-induced apoptosis, acting non-redundantly. Bak initiates cytochrome c release, while Bax activates caspases, highlighting their distinct roles in cell death.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Mitochondrial outer membrane permeabilization (MOMP) is a key event in apoptosis, involving the release of proteins like cytochrome c.
  • The proapoptotic proteins Bak and Bax were previously considered functionally redundant in mediating MOMP.

Purpose of the Study:

  • To investigate the functional redundancy of Bak and Bax in Neisseria gonorrhoeae (Ngo)- and cisplatin-induced apoptosis.
  • To elucidate the distinct roles of Bak and Bax in caspase activation and cytochrome c release during apoptosis.

Main Methods:

  • Silencing of Bak or Bax genes.
  • Induction of apoptosis using Ngo infection, cisplatin, or TNF-alpha.
  • Assessment of cytochrome c release and caspase activation.

Main Results:

  • Bak and Bax are functionally non-redundant in Ngo- and cisplatin-induced apoptosis.
  • Bak activation is caspase-independent, while Bax activation requires Bak and active caspases.
  • Bak is essential for cytochrome c release, and Bax is required for effector caspase activation.

Conclusions:

  • Bak and Bax play distinct, non-redundant roles in DNA damage and Ngo-induced apoptosis.
  • Both proteins are necessary for the complete apoptotic pathway, with Bak initiating mitochondrial events and Bax driving caspase execution.

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