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Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3

H Li1, S K Kolluri, J Gu

  • 1The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.

Science (New York, N.Y.)
|August 19, 2000
PubMed

Insights

TR3, a nuclear transcription factor, initiates apoptosis by moving to mitochondria. This mitochondrial translocation, not DNA binding, is key for its cell death-inducing function.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • TR3 is an immediate-early response gene and a transcription factor.
  • TR3 belongs to the steroid-thyroid hormone-retinoid receptor superfamily.
  • TR3 regulates apoptosis via an unknown mechanism.

Purpose of the Study:

  • To elucidate the mechanism by which TR3 regulates apoptosis.
  • To investigate the role of TR3 translocation in apoptosis.

Main Methods:

  • Studying the cellular localization of TR3.
  • Analyzing the effect of TR3 translocation on apoptosis.
  • Assessing the necessity of DNA binding and transactivation for TR3's proapoptotic function.

Main Results:

  • TR3 translocates from the nucleus to mitochondria in response to apoptotic stimuli.
  • Mitochondrial translocation of TR3 induces cytochrome c release and apoptosis.
  • TR3's proapoptotic effect is dependent on mitochondrial targeting, not DNA binding or transactivation.

Conclusions:

  • TR3 initiates apoptosis by translocating to mitochondria.
  • Nuclear transcription factors can translocate to mitochondria to trigger apoptosis.
  • Mitochondrial targeting is a critical mechanism for TR3-induced cell death.

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