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Related Experiment Videos

Constitutively active Galphaq and Galpha13 trigger apoptosis through different pathways

H Althoefer1, P Eversole-Cire, M I Simon

  • 1Division of Biology, California Institute of Technology, Pasadena, California 91125, USA.

The Journal of Biological Chemistry
|September 26, 1997
PubMed
Summary
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Constitutively active Galphaq and Galpha13 mutants induce apoptosis, a form of programmed cell death, through distinct signaling pathways. Overexpression of bcl-2 effectively blocks this apoptosis, regardless of cell culture conditions.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • G proteins are key regulators of cellular signaling pathways.
  • Aberrant G protein signaling can contribute to various cellular dysfunctions, including uncontrolled cell death.
  • Understanding the specific roles of G protein subunits in cell fate is crucial for deciphering cellular regulation.

Purpose of the Study:

  • To investigate the impact of constitutively active Galphaq and Galpha13 mutants on cell survival.
  • To elucidate the distinct signaling pathways by which Galphaq and Galpha13 induce apoptosis.
  • To determine the role of bcl-2 in modulating G protein-mediated apoptosis.

Main Methods:

  • Transfection of constitutively active Galphaq and Galpha13 mutants into cell lines.

Related Experiment Videos

  • Analysis of cellular phenotypes, including DNA condensation and nuclear fragmentation.
  • Flow cytometry for DNA fragmentation analysis.
  • Investigation of signaling pathways involving protein kinase C and Rho GTPase.
  • Assessment of apoptosis inhibition by bcl-2 overexpression.

    • Main Results:

    • Expression of constitutively active Galphaq and Galpha13 induced hallmarks of apoptosis, such as DNA condensation and nuclear fragmentation.
    • Galphaq triggered apoptosis via a protein kinase C-dependent pathway.
    • Galpha13 induced apoptosis through a pathway involving Rho GTPase activation.
    • Overexpression of bcl-2 successfully inhibited apoptosis induced by both Galphaq and Galpha13.
    • Apoptosis was observed in both high-serum and defined medium conditions, indicating a robust induction mechanism.

    Conclusions:

    • Constitutively active Galphaq and Galpha13 mutants are potent inducers of apoptosis.
    • Distinct signaling cascades mediate Galphaq- and Galpha13-induced programmed cell death.
    • The anti-apoptotic protein bcl-2 can effectively counteract G protein-mediated apoptosis.
    • These findings highlight the critical role of specific G protein subunits in regulating cell survival and death pathways.