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S. cerevisiae Strain Lacking Mitochondrial IF3 Shows Increased Levels of Tma19p during Adaptation to Respiratory Growthстатья
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 19 декабря 2019 г.
- Авторы: Sergey Levitskii, Baleva Maria V., Ivan Chicherin, Krasheninnikov Igor A., Piotr Kamenski
- Журнал: Cells
- Том: 8
- Год издания: 2019
- Издательство: MDPI
- Местоположение издательства: Basel, Switzerland
- Первая страница: 645
- DOI: 10.3390/cells8070645
- Аннотация: After billions of years of evolution, mitochondrion retains its own genome, which getsexpressed in mitochondrial matrix. Mitochondrial translation machinery rather differs frommodern bacterial and eukaryotic cytosolic systems. Any disturbance in mitochondrial translationdrastically impairs mitochondrial function. In budding yeast Saccharomyces cerevisiae, deletion ofthe gene coding for mitochondrial translation initiation factor 3 - AIM23, leads to an imbalance inmitochondrial protein synthesis and significantly delays growth after shifting from fermentable tonon-fermentable carbon sources. Molecular mechanism underlying this adaptation to respiratorygrowth was unknown. Here, we demonstrate that slow adaptation from glycolysis to respiration inthe absence of Aim23p is accompanied by a gradual increase of cytochrome c oxidase activity andby increased levels of Tma19p protein, which protects mitochondria from oxidative stress.
- Добавил в систему: Левицкий Сергей Алексеевич