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...

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Bibliographic Details
Published in:Open biology 2021-04, Vol.11 (4), p.200369-200369
Main Authors: Uehara, Lisa, Saitoh, Shigeaki, Mori, Ayaka, Sajiki, Kenichi, Toyoda, Yusuke, Masuda, Fumie, Soejima, Saeko, Tahara, Yuria, Yanagida, Mitsuhiro
Format: Article
Language:English
Subjects:
Energy Metabolism
fatty acid synthesis
Gene Expression Profiling
Gene Expression Regulation, Fungal
Genes, Essential
Humans
mitochondria
Mitochondrial Proteins - genetics
Mitochondrial Proteins - metabolism
Mutation
nutritional stress
Phenotype
ribosome
RNA processing
Schizosaccharomyces - physiology
Schizosaccharomyces pombe Proteins - genetics
Schizosaccharomyces pombe Proteins - metabolism
Stress, Physiological
ts mutants
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Summary: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 , 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 ( ) 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 mitochondrial mutations may cause defects of gene expression in the mitochondrial genome. and are defective in mitochondrial ribosomal proteins. is defective in rRNA expression, and and 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.
ISSN:2046-2441
2046-2441
DOI:10.1098/rsob.200369