Inhibition of mitochondrial genome expression triggers the activation of CHOP-10 by a cell signaling dependent on the integrated stress response but not the mitochondrial unfolded protein response

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Abstract

Mitochondria-to-nucleus communication, known as retrograde signaling, is important to adjust the nuclear gene expression in response to organelle dysfunction. Among the transcription factors described to respond to mitochondrial stress, CHOP-10 is activated by respiratory chain inhibition, mitochondrial accumulation of unfolded proteins and mtDNA mutations. In this study, we show that altered/impaired expression of mtDNA induces CHOP-10 expression in a signaling pathway that depends on the eIF2α/ATF4 axis of the integrated stress response rather than on the mitochondrial unfolded protein response.

Original languageEnglish
Pages (from-to)58-68
Number of pages11
JournalMitochondrion
Volume21
Early online date30 Jan 2015
DOIs
Publication statusPublished - 1 Mar 2015

Keywords

  • C/EBP homologous protein 10 (CHOP-10)
  • Doxycycline
  • Integrated stress response (ISR)
  • Mitochondria unfolded protein response (mtUPR)
  • Mitochondrial dysfunction
  • MtDNA depletion

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