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Adaptive expression responses in the Pol-γ null strain of S. pombe depleted of mitochondrial genome
BACKGROUND: DNA polymerase γ(Pol-γ) has been shown to be essential for maintenance of the mitochondrial genome (mtDNA) in the petite-positive budding yeast Saccharomyces cerevisiae. Budding yeast cells lacking mitochondria exhibit a slow-growing or petite-colony phenotype. Petite strains fail to gro...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2045682/ https://www.ncbi.nlm.nih.gov/pubmed/17868468 http://dx.doi.org/10.1186/1471-2164-8-323 |
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author | Chu, Zhaoqing Li, Juntao Eshaghi, Majid Karuturi, R Krishna Murthy Lin, Kui Liu, Jianhua |
author_facet | Chu, Zhaoqing Li, Juntao Eshaghi, Majid Karuturi, R Krishna Murthy Lin, Kui Liu, Jianhua |
author_sort | Chu, Zhaoqing |
collection | PubMed |
description | BACKGROUND: DNA polymerase γ(Pol-γ) has been shown to be essential for maintenance of the mitochondrial genome (mtDNA) in the petite-positive budding yeast Saccharomyces cerevisiae. Budding yeast cells lacking mitochondria exhibit a slow-growing or petite-colony phenotype. Petite strains fail to grow on non-fermentable carbon sources. However, it is not clear whether the Pol-γ is required for mtDNA maintenance in the petite-negative fission yeast Schizosaccharomyces pombe. RESULTS: We show that disruption of the nuclear gene pog1(+ )that encodes Pol-γ is sufficient to deplete mtDNA in S. pombe. Cells bearing pog1Δ allele require substantial growth periods to form petite colonies. Mitotracker assays indicate that pog1Δ cells are defective in mitochondrial function and EM analyses suggest that pog1Δ cells lack normal mitochondrial structures. Depletion of mtDNA in pog1Δ cells is evident from quantitative real-time PCR assays. Genome-wide expression profiles of pog1Δ and other mtDNA-less cells reveal that many genes involved in response to stimulus, energy derivation by oxidation of organic compounds, cellular carbohydrate metabolism, and energy reserve metabolism are induced. Conversely, many genes encoding proteins involved in amino acid metabolism and oxidative phosphorylation are repressed. CONCLUSION: By showing that Pol-γ is essential for mtDNA maintenance and disruption of pog1(+ )alters the genome-wide expression profiles, we demonstrated that cells lacking mtDNA exhibit adaptive nuclear gene expression responses in the petite-negative S. pombe. |
format | Text |
id | pubmed-2045682 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-20456822007-10-31 Adaptive expression responses in the Pol-γ null strain of S. pombe depleted of mitochondrial genome Chu, Zhaoqing Li, Juntao Eshaghi, Majid Karuturi, R Krishna Murthy Lin, Kui Liu, Jianhua BMC Genomics Research Article BACKGROUND: DNA polymerase γ(Pol-γ) has been shown to be essential for maintenance of the mitochondrial genome (mtDNA) in the petite-positive budding yeast Saccharomyces cerevisiae. Budding yeast cells lacking mitochondria exhibit a slow-growing or petite-colony phenotype. Petite strains fail to grow on non-fermentable carbon sources. However, it is not clear whether the Pol-γ is required for mtDNA maintenance in the petite-negative fission yeast Schizosaccharomyces pombe. RESULTS: We show that disruption of the nuclear gene pog1(+ )that encodes Pol-γ is sufficient to deplete mtDNA in S. pombe. Cells bearing pog1Δ allele require substantial growth periods to form petite colonies. Mitotracker assays indicate that pog1Δ cells are defective in mitochondrial function and EM analyses suggest that pog1Δ cells lack normal mitochondrial structures. Depletion of mtDNA in pog1Δ cells is evident from quantitative real-time PCR assays. Genome-wide expression profiles of pog1Δ and other mtDNA-less cells reveal that many genes involved in response to stimulus, energy derivation by oxidation of organic compounds, cellular carbohydrate metabolism, and energy reserve metabolism are induced. Conversely, many genes encoding proteins involved in amino acid metabolism and oxidative phosphorylation are repressed. CONCLUSION: By showing that Pol-γ is essential for mtDNA maintenance and disruption of pog1(+ )alters the genome-wide expression profiles, we demonstrated that cells lacking mtDNA exhibit adaptive nuclear gene expression responses in the petite-negative S. pombe. BioMed Central 2007-09-15 /pmc/articles/PMC2045682/ /pubmed/17868468 http://dx.doi.org/10.1186/1471-2164-8-323 Text en Copyright © 2007 Chu et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Chu, Zhaoqing Li, Juntao Eshaghi, Majid Karuturi, R Krishna Murthy Lin, Kui Liu, Jianhua Adaptive expression responses in the Pol-γ null strain of S. pombe depleted of mitochondrial genome |
title | Adaptive expression responses in the Pol-γ null strain of S. pombe depleted of mitochondrial genome |
title_full | Adaptive expression responses in the Pol-γ null strain of S. pombe depleted of mitochondrial genome |
title_fullStr | Adaptive expression responses in the Pol-γ null strain of S. pombe depleted of mitochondrial genome |
title_full_unstemmed | Adaptive expression responses in the Pol-γ null strain of S. pombe depleted of mitochondrial genome |
title_short | Adaptive expression responses in the Pol-γ null strain of S. pombe depleted of mitochondrial genome |
title_sort | adaptive expression responses in the pol-γ null strain of s. pombe depleted of mitochondrial genome |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2045682/ https://www.ncbi.nlm.nih.gov/pubmed/17868468 http://dx.doi.org/10.1186/1471-2164-8-323 |
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