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Cited by 25Mitochondrial Function and PathologyAutophagy in Disease and TherapyCancer, Hypoxia, and Metabolism

Adaptive responses to mitochondrial dysfunction in the ρ° Namalwa cell

Behan, Áine, Doyle, Sineaid, Farrell, Michael·2005·Mitochondrion
DOI 10.1016/j.mito.2005.03.002
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Abstract

Mitochondrial function depends on the synchronised expression of nuclear and mitochondrial-encoded genes. The expression of many nuclear genes is sensitive to the functional state of mitochondria. Mitochondria containing mutated mtDNA populations have been shown to withstand stress to a high level of tolerance. The prolonged survival of cells that are devoid of mitochondrial DNA is further evidence for the existence of this adaptive response. Yeast cells lacking the mitochondrial genome configure their pattern of nuclear gene expression to accommodate changes in nutrient availability and in response to different stress conditions. Little is known about the signalling pathways that mediate the adaptive response in mammalian cells with mitochondrial dysfunction. To gain a global perspective on adaptive responses in cells with mitochondrial dysfunction, we used Affymetrix microarray technology to compare the whole genome transcription profile of Namalwa cells (rho(+)) to that of a Namalwa cell depleted of mitochondrial DNA (rho degrees ). Our results demonstrate that rho degrees Namalwa induce genes encoding hypoxia target proteins, mitochondrial ribosomal proteins, transport channels, tRNA synthetases and enzymes of the glycolytic pathway and the fatty oxidation pathway suggesting that hypoxia and the ensuing cellular adaptations could play an important adaptive role in cells with mitochondrial dysfunction.

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  • Both ρ0 and cybridisation processes can cause significant and stable up-regulation of many nuclear transcripts involved in OXPHOS, even after repopulation of ρ0 cells with wild-type mitochondria.

    “Indeed, microarray studies have demonstrated that both processes can cause significant and stable up-regulation of many nuclear transcripts involved in OXHOS, even after repopulation of ρ 0 cells with wild-type mitochondria [157,158].”

    From Mitochondrial DNA mutations and human disease (2010) · cites this paper as [157]

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Authors
Behan, Á., Doyle, S., & Farrell, M.
Affiliations
  • Royal College of Surgeons in Ireland (IE)
  • Beaumont Hospital (IE)
Corresponding author
Behan, Áine
Venue
Mitochondrion
Publisher
Elsevier BV
Published
2005-06
Volume
5
Issue
3
Pages
173-193
ISSN
1567-7249 (ISSN-L)
DOI
10.1016/j.mito.2005.03.002
OpenAlex
W2055758074
Cited by
25
References
39
Citations by year
2026: 1 · 2022: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2014: 2 · 2013: 2 · 2012: 2
FWCI
1.13
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Mitochondrion (publishedVersion)
  • PubMed (publishedVersion)
Funders
Royal College of Surgeons in Ireland
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Keywords
mitochondrial dysfunction, adaptive response, mitochondrial DNA deletions, rho0 cells, Namalwa cells, hypoxia, gene expression profiling, mitochondrial ribosomal proteins, tRNA synthetase, glycolysis, fatty acid oxidation, stress tolerance
MeSH terms
Adaptation, Physiological, Adenosine Triphosphatases, Cobalt, DNA-Binding Proteins, DNA, Mitochondrial, Ethidium, Humans, Kinetics, Mitochondria, Nuclear Proteins, Oxidative Phosphorylation, Transcription Factors, Transcription, Genetic, Cell Hypoxia, Gene Expression Regulation, Neoplastic, Polymerase Chain Reaction, Cell Culture Techniques, Oligonucleotide Array Sequence Analysis, Mitochondrial Proteins, Cell Line, Tumor, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor 1, alpha Subunit

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