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Multiple nutritional phenotypes of fission yeast mutants defective in genes encoding essential mitochondrial proteins
Mitochondria are essential for regulation of cellular respiration, energy production, small molecule metabolism, anti-oxidation and cell ageing, among other things. While the mitochondrial genome contains a small number of protein-coding genes, the great majority of mitochondrial proteins are encode...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Royal Society
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8025305/ https://www.ncbi.nlm.nih.gov/pubmed/33823662 http://dx.doi.org/10.1098/rsob.200369 |
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author | Uehara, Lisa Saitoh, Shigeaki Mori, Ayaka Sajiki, Kenichi Toyoda, Yusuke Masuda, Fumie Soejima, Saeko Tahara, Yuria Yanagida, Mitsuhiro |
author_facet | Uehara, Lisa Saitoh, Shigeaki Mori, Ayaka Sajiki, Kenichi Toyoda, Yusuke Masuda, Fumie Soejima, Saeko Tahara, Yuria Yanagida, Mitsuhiro |
author_sort | Uehara, Lisa |
collection | PubMed |
description | Mitochondria are essential for regulation of cellular respiration, energy production, small molecule metabolism, anti-oxidation and cell ageing, among other things. While the mitochondrial genome contains a small number of protein-coding genes, the great majority of mitochondrial proteins are encoded by chromosomal genes. In the fission yeast Schizosaccharomyces pombe, 770 proteins encoded by chromosomal genes are located in mitochondria. Of these, 195 proteins, many of which are implicated in translation and transport, are absolutely essential for viability. We isolated and characterized eight temperature-sensitive (ts) strains with mutations in essential mitochondrial proteins. Interestingly, they are also sensitive to limited nutrition (glucose and/or nitrogen), producing low-glucose-sensitive and ‘super-housekeeping' phenotypes. They fail to produce colonies under low-glucose conditions at the permissive temperature or lose cell viability under nitrogen starvation at the restrictive temperature. The majority of these ts mitochondrial mutations may cause defects of gene expression in the mitochondrial genome. mrp4 and mrp17 are defective in mitochondrial ribosomal proteins. ppr3 is defective in rRNA expression, and trz2 and vrs2 are defective in tRNA maturation. This study promises potentially large dividends because mitochondrial quiescent functions are vital for human brain and muscle, and also for longevity. |
format | Online Article Text |
id | pubmed-8025305 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | The Royal Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-80253052021-04-16 Multiple nutritional phenotypes of fission yeast mutants defective in genes encoding essential mitochondrial proteins Uehara, Lisa Saitoh, Shigeaki Mori, Ayaka Sajiki, Kenichi Toyoda, Yusuke Masuda, Fumie Soejima, Saeko Tahara, Yuria Yanagida, Mitsuhiro Open Biol Research Mitochondria are essential for regulation of cellular respiration, energy production, small molecule metabolism, anti-oxidation and cell ageing, among other things. While the mitochondrial genome contains a small number of protein-coding genes, the great majority of mitochondrial proteins are encoded by chromosomal genes. In the fission yeast Schizosaccharomyces pombe, 770 proteins encoded by chromosomal genes are located in mitochondria. Of these, 195 proteins, many of which are implicated in translation and transport, are absolutely essential for viability. We isolated and characterized eight temperature-sensitive (ts) strains with mutations in essential mitochondrial proteins. Interestingly, they are also sensitive to limited nutrition (glucose and/or nitrogen), producing low-glucose-sensitive and ‘super-housekeeping' phenotypes. They fail to produce colonies under low-glucose conditions at the permissive temperature or lose cell viability under nitrogen starvation at the restrictive temperature. The majority of these ts mitochondrial mutations may cause defects of gene expression in the mitochondrial genome. mrp4 and mrp17 are defective in mitochondrial ribosomal proteins. ppr3 is defective in rRNA expression, and trz2 and vrs2 are defective in tRNA maturation. This study promises potentially large dividends because mitochondrial quiescent functions are vital for human brain and muscle, and also for longevity. The Royal Society 2021-04-07 /pmc/articles/PMC8025305/ /pubmed/33823662 http://dx.doi.org/10.1098/rsob.200369 Text en © 2021 The Authors. https://creativecommons.org/licenses/by/4.0/Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, provided the original author and source are credited. |
spellingShingle | Research Uehara, Lisa Saitoh, Shigeaki Mori, Ayaka Sajiki, Kenichi Toyoda, Yusuke Masuda, Fumie Soejima, Saeko Tahara, Yuria Yanagida, Mitsuhiro Multiple nutritional phenotypes of fission yeast mutants defective in genes encoding essential mitochondrial proteins |
title | Multiple nutritional phenotypes of fission yeast mutants defective in genes encoding essential mitochondrial proteins |
title_full | Multiple nutritional phenotypes of fission yeast mutants defective in genes encoding essential mitochondrial proteins |
title_fullStr | Multiple nutritional phenotypes of fission yeast mutants defective in genes encoding essential mitochondrial proteins |
title_full_unstemmed | Multiple nutritional phenotypes of fission yeast mutants defective in genes encoding essential mitochondrial proteins |
title_short | Multiple nutritional phenotypes of fission yeast mutants defective in genes encoding essential mitochondrial proteins |
title_sort | multiple nutritional phenotypes of fission yeast mutants defective in genes encoding essential mitochondrial proteins |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8025305/ https://www.ncbi.nlm.nih.gov/pubmed/33823662 http://dx.doi.org/10.1098/rsob.200369 |
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