Large Functional Range of Steady-State Levels of Nuclear and Mitochondrial Transcripts Coding for the Subunits of the Human Mitochondrial OXPHOS System

  1. Hervé Duborjal1,
  2. Réjane Beugnot1,2,
  3. Bénédicte Mousson de Camaret3, and
  4. Jean-Paul Issartel1,4
  1. 1GENOME Express SA, 38944 Meylan, France; 2UMR 5090 CNRS-DRDC, CEA Grenoble, 38054 Grenoble, cedex 9, France; 3Laboratoire de Biochimie, Hôpital Debrousse, 69322 Lyon, France

Abstract

We have measured, by reverse transcription and real-time quantitative PCR, the steady-state levels of the mitochondrial and nuclear transcripts encoding several subunits of the human oxidative phosphorylation (OXPHOS) system, in different normal tissues (muscle, liver, trachea, and kidney) and in cultured cells (normal fibroblasts, 143B osteosarcoma cells, 143B206 ρ0 cells). Five mitochondrial transcripts and nine nuclear transcripts were assessed. The measured amounts of these OXPHOS transcripts in muscle samples corroborated data obtained by others using the serial analysis of gene expression (SAGE) method to appraise gene expression in the same type of tissue. Steady-state levels for all the transcripts were found to range over more than two orders of magnitude. Most of the time, the mitochondrial H-strand transcripts were present at higher levels than the nuclear transcripts. The mitochondrial L-strand transcript ND6 was usually present at a low level. Cultured 143B cells contained significantly reduced amounts of mitochondrial transcripts in comparison with the tissue samples. In 143B206 ρ0 cells, fully depleted of mitochondrial DNA, the levels of nuclear OXPHOS transcripts were not modified in comparison with the parental cells. This observation indicated that nuclear transcription is not coordinated with mitochondrial transcription. We also observed that in the different tissues and cells, there is a transcriptional coregulation of all the investigated nuclear genes. Nuclear OXPHOS gene expression seems to be finely regulated.

[The following individual kindly provided reagents, samples, or unpublished information as indicated in the paper: G. Attardi.]

Footnotes

  • 4 Corresponding author.

  • E-MAIL j.issartel{at}genomex.com; FAX (33) 4 56 38 11 00.

  • Article and publication are at http://www.genome.org/cgi/doi/10.1101/gr.194102.

    • Received February 19, 2002.
    • Accepted October 8, 2002.
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