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Analysis of the Expression and Complexes Assembly of the Mitochondrial Respiratory Chain Proteins in the Fission Yeast Schizosaccharomyces pombe
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Gene expression profiling identifies a role for CHOP during inhibition of the mitochondrial respiratory chain

Fumihiro Ishikawa1, Takashi Akimoto, Haruka Yamamoto

  • 1Department of Microbiology, Showa University School of Pharmacy, Tokyo, Japan.

Journal of Biochemistry
|March 24, 2009
PubMed

Insights

Mitochondrial dysfunction triggers stress responses. CHOP-10 regulates gene expression during mitochondrial stress, mitigating xenobiotic toxicity.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Toxicology

Background:

  • Mitochondrial dysfunction, particularly respiratory chain interference, underlies xenobiotic toxicity.
  • Understanding cellular responses to mitochondrial stress is crucial for toxicology and drug development.

Purpose of the Study:

  • To investigate gene expression changes induced by pharmacological inhibition of the mitochondrial respiratory chain.
  • To elucidate the role of transcription factor CHOP-10 in mediating cellular responses to mitochondrial stress.

Main Methods:

  • DNA microarray analysis of cells treated with rotenone or antimycin A to inhibit respiratory chain complexes I and III.
  • siRNA-mediated knockdown of CHOP-10 to assess its role in gene regulation and cytotoxicity.

Main Results:

  • Pharmacological inhibition of the respiratory chain resulted in significant up- or down-regulation of 48 genes.
  • CHOP-10 was identified as a key transcriptional regulator, mediating the up-regulation of several stress- and metabolic-related genes.
  • CHOP-10 knockdown attenuated cytotoxicity caused by mitochondrial respiratory chain inhibition.

Conclusions:

  • CHOP-10 plays a critical role in coordinating gene expression responses to mitochondrial stress.
  • The signaling pathway for Trib3 induction during mitochondrial stress differs from that during ER stress.
  • Targeting CHOP-10 may offer a therapeutic strategy to mitigate xenobiotic-induced mitochondrial toxicity.

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