Loss of p53 causes mitochondrial DNA depletion and altered mitochondrial reactive oxygen species homeostasis
In addition to its central role in cellular stress signaling, the tumor suppressor p53 modulates mitochondrial respiration through its nuclear transcription factor activity and localizes to mitochondria, where it enhances apoptosis and suppresses mitochondrial DNA (mtDNA) mutagenesis. Here we demons...
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| Vydané v: | Biochimica et biophysica acta Ročník 1787; číslo 5; s. 328 - 334 |
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| Hlavní autori: | , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Netherlands
Elsevier B.V
01.05.2009
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| ISSN: | 0005-2728, 0006-3002, 1879-2650 |
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| Abstract | In addition to its central role in cellular stress signaling, the tumor suppressor p53 modulates mitochondrial respiration through its nuclear transcription factor activity and localizes to mitochondria, where it enhances apoptosis and suppresses mitochondrial DNA (mtDNA) mutagenesis. Here we demonstrate a new conserved role for p53 in mtDNA copy number maintenance and mitochondrial reactive oxygen species (ROS) homeostasis. In mammals, mtDNA is present at thousands of copies per cell and is essential for normal development and cell function. We show that p53 null mouse and p53 knockdown human primary fibroblasts exhibit mtDNA depletion and decreased mitochondrial mass under normal culture growth conditions. This is accompanied by a reduction of the p53R2 subunit of ribonucleotide reductase mRNA and protein and of mitochondrial transcription factor A (mtTFA) at the protein level only. Finally, p53-depleted cells exhibit significant disruption of cellular ROS homeostasis, characterized by reduced mitochondrial and cellular superoxide levels and increased cellular hydrogen peroxide. Altogether, these results elucidate additional mitochondria-related functions for p53 and implicate mtDNA depletion and ROS alterations as potentially relevant to cellular transformation, cancer cell phenotypes, and the Warburg Effect. |
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| AbstractList | In addition to its central role in cellular stress signaling, the tumor suppressor p53 modulates mitochondrial respiration through its nuclear transcription factor activity and localizes to mitochondria, where it enhances apoptosis and suppresses mitochondrial DNA (mtDNA) mutagenesis. Here we demonstrate a new conserved role for p53 in mtDNA copy number maintenance and mitochondrial reactive oxygen species (ROS) homeostasis. In mammals, mtDNA is present at thousands of copies per cell and is essential for normal development and cell function. We show that p53 null mouse and p53 knockdown human primary fibroblasts exhibit mtDNA depletion and decreased mitochondrial mass under normal culture growth conditions. This is accompanied by a reduction of the p53R2 subunit of ribonucleotide reductase mRNA and protein and of mitochondrial transcription factor A (mtTFA) at the protein level only. Finally, p53-depleted cells exhibit significant disruption of cellular ROS homeostasis, characterized by reduced mitochondrial and cellular superoxide levels and increased cellular hydrogen peroxide. Altogether, these results elucidate additional mitochondria-related functions for p53 and implicate mtDNA depletion and ROS alterations as potentially relevant to cellular transformation, cancer cell phenotypes, and the Warburg Effect. |
| Author | Eaton, Jana S. Lebedeva, Maria A. Shadel, Gerald S. |
| Author_xml | – sequence: 1 givenname: Maria A. surname: Lebedeva fullname: Lebedeva, Maria A. organization: Department of Pathology, Yale University School of Medicine, 310 Cedar Street, P.O. Box 208023, New Haven, CT 06520-8023, USA – sequence: 2 givenname: Jana S. surname: Eaton fullname: Eaton, Jana S. organization: Department of Pathology, Yale University School of Medicine, 310 Cedar Street, P.O. Box 208023, New Haven, CT 06520-8023, USA – sequence: 3 givenname: Gerald S. surname: Shadel fullname: Shadel, Gerald S. email: gerald.shadel@yale.edu organization: Department of Pathology, Yale University School of Medicine, 310 Cedar Street, P.O. Box 208023, New Haven, CT 06520-8023, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19413947$$D View this record in MEDLINE/PubMed |
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| Keywords | Mitochondrial transcription factor A Reactive oxygen species mtDNA depletion p53R2 p53 Cancer |
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| SubjectTerms | Animals Cancer DNA Primers DNA, Mitochondrial - genetics Fibroblasts - cytology Fibroblasts - physiology Gene Deletion Homeostasis Humans Membrane Potentials Mice Mice, Inbred C57BL Mice, Knockout Mitochondria - metabolism Mitochondria - physiology Mitochondrial transcription factor A mtDNA depletion Oxidative Phosphorylation p53 p53R2 Polymerase Chain Reaction Reactive oxygen species Reactive Oxygen Species - metabolism RNA, Messenger - genetics Transcription, Genetic Tumor Suppressor Protein p53 - deficiency Tumor Suppressor Protein p53 - genetics |
| Title | Loss of p53 causes mitochondrial DNA depletion and altered mitochondrial reactive oxygen species homeostasis |
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