Bid regulation of neuronal apoptosis

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Published on: August 9, 2014

J R Leonard1, C D'Sa, B R Cahn

  • 1Department of Neurological Surgery, Washington University School of Medicine, 660 S. Euclid Avenue Box 8118, St. Louis, MO 63110, USA.

Brain Research. Developmental Brain Research
|June 20, 2001
PubMed

Insights

Bid protein does not appear essential for neuronal cell death during development or in response to toxins. Bid-deficient embryos showed normal development and neuronal apoptosis, indicating no crucial role for Bid in these processes.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Bid is a pro-apoptotic protein in the Bcl-2 family, known to interact with Bax.
  • Bax deficiency leads to reduced neuronal apoptosis in vivo and in vitro.
  • The role of Bid in neuronal cell death remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of Bid in neurodevelopment and neuronal apoptosis.
  • To determine if Bid-deficiency affects naturally occurring or genotoxin-induced neuronal cell death.

Main Methods:

  • Analysis of Bid-deficient embryos for neurodevelopmental abnormalities.
  • In vitro apoptosis assays using telencephalic neural precursor cells and neurons.
  • Exposure to cytosine arabinoside (AraC) to induce apoptosis.

Main Results:

  • Bid-deficient embryos exhibited no observable neurodevelopmental abnormalities.
  • Bid-deficiency did not alter the apoptotic response of neural precursor cells or neurons to AraC.
  • No significant difference in neuronal cell death was observed between wild-type and Bid-deficient models.

Conclusions:

  • Bid does not play a critical role in embryonic neurodevelopment.
  • Bid is not essential for genotoxin-induced neuronal apoptosis.
  • The study concludes that Bid is not required for naturally occurring or induced neuronal cell death.

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