Loss of dE2F compromises mitochondrial function

Dev Cell. 2013 Nov 25;27(4):438-51. doi: 10.1016/j.devcel.2013.10.002.

Abstract

E2F/DP transcription factors regulate cell proliferation and apoptosis. Here, we investigated the mechanism of the resistance of Drosophila dDP mutants to irradiation-induced apoptosis. Contrary to the prevailing view, this is not due to an inability to induce the apoptotic transcriptional program, because we show that this program is induced; rather, this is due to a mitochondrial dysfunction of dDP mutants. We attribute this defect to E2F/DP-dependent control of expression of mitochondria-associated genes. Genetic attenuation of several of these E2F/DP targets mimics the dDP mutant mitochondrial phenotype and protects against irradiation-induced apoptosis. Significantly, the role of E2F/DP in the regulation of mitochondrial function is conserved between flies and humans. Thus, our results uncover a role of E2F/DP in the regulation of mitochondrial function and demonstrate that this aspect of E2F regulation is critical for the normal induction of apoptosis in response to irradiation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Genetically Modified
  • Apoptosis*
  • Blotting, Western
  • Bone Neoplasms / genetics
  • Bone Neoplasms / metabolism
  • Bone Neoplasms / pathology
  • Cell Cycle
  • Cell Proliferation
  • Chromatin Immunoprecipitation
  • DNA Damage / genetics
  • DNA Damage / radiation effects
  • Drosophila Proteins / genetics
  • Drosophila Proteins / metabolism*
  • Drosophila melanogaster / genetics
  • Drosophila melanogaster / growth & development
  • Drosophila melanogaster / metabolism*
  • E2F Transcription Factors / genetics
  • E2F Transcription Factors / metabolism*
  • Fluorescent Antibody Technique
  • Gamma Rays
  • Humans
  • Immunoenzyme Techniques
  • Mitochondria / metabolism
  • Mitochondria / pathology*
  • Mitochondria / radiation effects
  • Osteosarcoma / genetics
  • Osteosarcoma / metabolism
  • Osteosarcoma / pathology*
  • Phenotype
  • Trans-Activators / genetics
  • Trans-Activators / metabolism*
  • Transcription Factors
  • Tumor Cells, Cultured

Substances

  • Dp transcription factor, Drosophila
  • Drosophila Proteins
  • E2F Transcription Factors
  • E2f1 protein, Drosophila
  • Trans-Activators
  • Transcription Factors