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Opposing roles for ATF2 and c-Fos in c-Jun-mediated neuronal apoptosis

Zhongmin Yuan1, Shoufang Gong, Jingyan Luo

  • 1Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, 74 Zhongshan Road II, Guangzhou, China.

Molecular and Cellular Biology
|March 4, 2009
PubMed

Insights

Activating transcription factor-2 (ATF2) and c-Fos regulate activator protein 1 (AP-1) transcription factor c-Jun

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • The transcription factor c-Jun (an activator protein 1 component) is vital for neuronal apoptosis.
  • The specific dimerization partners and regulatory mechanisms of c-Jun in neuronal apoptosis are not fully understood.

Purpose of the Study:

  • To investigate the dimerization partners and regulatory mechanisms of c-Jun during neuronal apoptosis.
  • To elucidate the roles of activating transcription factor-2 (ATF2) and c-Fos in c-Jun-mediated neuronal cell death.

Main Methods:

  • Utilized dominant-negative mutants, small hairpin RNAs, and decoy oligonucleotides to inhibit c-Jun/ATF2 heterodimerization.
  • Employed bimolecular fluorescence complementation (BiFC) assays to study heterodimerization in living neurons.
  • Performed chromatin immunoprecipitation (ChIP) assays to assess protein binding to DNA.

Main Results:

  • c-Jun-mediated neuronal apoptosis requires both ATF2 activation and c-Fos downregulation.
  • c-Jun predominantly heterodimerizes with ATF2, forming a complex that enhances apoptosis by triggering ATF activity.
  • c-Fos downregulation promotes c-Jun/ATF2 heterodimerization, while c-Fos expression inhibits this complex formation and its downstream target gene expression, thereby suppressing apoptosis.

Conclusions:

  • Potassium deprivation-induced neuronal apoptosis involves increased c-Jun/ATF2 heterodimerization and decreased c-Fos expression.
  • ATF2 and c-Fos play opposing roles in c-Jun-mediated neuronal apoptosis, with ATF2 promoting and c-Fos inhibiting the process.

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