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Minority potassium-uptake system Trk2 has a crucial role in yeast survival of glucose-induced cell death
M. Dušková, D. Cmunt, K. Papoušková, J. Masaryk, H. Sychrová
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
Odkazy
PubMed
34170815
DOI
10.1099/mic.0.001065
Knihovny.cz E-zdroje
- MeSH
- buněčná smrt MeSH
- draslík metabolismus MeSH
- glukosa metabolismus MeSH
- mikrobiální viabilita MeSH
- proteiny přenášející kationty genetika metabolismus MeSH
- Saccharomyces cerevisiae - proteiny genetika metabolismus MeSH
- Saccharomyces cerevisiae cytologie růst a vývoj metabolismus MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
The existence of programmed cell death in Saccharomyces cerevisiae has been reported for many years. Glucose induces the death of S. cerevisiae in the absence of additional nutrients within a few hours, and the absence of active potassium uptake makes cells highly sensitive to this process. S. cerevisiae cells possess two transporters, Trk1 and Trk2, which ensure a high intracellular concentration of potassium, necessary for many physiological processes. Trk1 is the major system responsible for potassium acquisition in growing and dividing cells. The contribution of Trk2 to potassium uptake in growing cells is almost negligible, but Trk2 becomes crucial for stationary cells for their survival of some stresses, e.g. anhydrobiosis. As a new finding, we show that both Trk systems contribute to the relative thermotolerance of S. cerevisiae BY4741. Our results also demonstrate that Trk2 is much more important for the cell survival of glucose-induced cell death than Trk1, and that stationary cells deficient in active potassium uptake lose their ATP stocks more rapidly than cells with functional Trk systems. This is probably due to the upregulated activity of plasma-membrane Pma1 H+-ATPase, and consequently, it is the reason why these cells die earlier than cells with functional active potassium uptake.
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- $a The existence of programmed cell death in Saccharomyces cerevisiae has been reported for many years. Glucose induces the death of S. cerevisiae in the absence of additional nutrients within a few hours, and the absence of active potassium uptake makes cells highly sensitive to this process. S. cerevisiae cells possess two transporters, Trk1 and Trk2, which ensure a high intracellular concentration of potassium, necessary for many physiological processes. Trk1 is the major system responsible for potassium acquisition in growing and dividing cells. The contribution of Trk2 to potassium uptake in growing cells is almost negligible, but Trk2 becomes crucial for stationary cells for their survival of some stresses, e.g. anhydrobiosis. As a new finding, we show that both Trk systems contribute to the relative thermotolerance of S. cerevisiae BY4741. Our results also demonstrate that Trk2 is much more important for the cell survival of glucose-induced cell death than Trk1, and that stationary cells deficient in active potassium uptake lose their ATP stocks more rapidly than cells with functional Trk systems. This is probably due to the upregulated activity of plasma-membrane Pma1 H+-ATPase, and consequently, it is the reason why these cells die earlier than cells with functional active potassium uptake.
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