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Nickel induced cell impairments are negatively regulated by the Tor1 kinase in Schizosaccharomyces pombe

In our study we investigated the effect of different nickel (NiSO 4 ·6H 2 O) (Ni) concentrations on cell division, cellular morphology and ionome homeostasis of the eukaryotic model organism Schizosaccharomyces pombe . Target of rapamycin (TOR) protein kinase is one of the key regulators of cell gro...

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Bibliographic Details
Published in:World journal of microbiology & biotechnology 2021-10, Vol.37 (10), p.165-165, Article 165
Main Authors: Navratilova, Alica, Kovar, Marek, Trakovicka, Anna, Pozgajova, Miroslava
Format: Article
Language:English
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Summary:In our study we investigated the effect of different nickel (NiSO 4 ·6H 2 O) (Ni) concentrations on cell division, cellular morphology and ionome homeostasis of the eukaryotic model organism Schizosaccharomyces pombe . Target of rapamycin (TOR) protein kinase is one of the key regulators of cell growth under different environmental stresses. We analyzed the effect of Ni on cell strains lacking the Tor1 signaling pathway utilizing light-absorbance spectroscopy, visualization, microscopy and inductively coupled plasma optical emission spectroscopy. Interestingly, our findings revealed that Ni mediated cell growth alterations are noticeably lower in Tor1 deficient cells. Greater size of Tor1 depleted cells reached similar quantitative parameters to wild type cells upon incubation with 400 μM Ni. Differences of ion levels among the two tested yeast strains were detected even before Ni addition. Addition of high concentration (1 mM) of the heavy metal, representing acute contamination, caused considerable changes in the ionome of both strains. Strikingly, Tor1 deficient cells displayed largely reduced Ni content after treatment compared to wild type controls (644.1 ± 49 vs. 2096.8 ± 75 μg/g), suggesting its significant role in Ni trafficking. Together our results predict yet undefined role for the Tor1 signaling in metal uptake and/or metabolism. Graphic abstract
ISSN:0959-3993
1573-0972
DOI:10.1007/s11274-021-03130-2