scholarly journals Identification of Genes Involved in the Toxic Response of Saccharomyces cerevisiae against Iron and Copper Overload by Parallel Analysis of Deletion Mutants

2008 ◽  
Vol 102 (1) ◽  
pp. 205-205 ◽  
Author(s):  
William J. Jo ◽  
Alex Loguinov ◽  
Michelle Chang ◽  
Henri Wintz ◽  
Corey Nislow ◽  
...  
2007 ◽  
Vol 101 (1) ◽  
pp. 140-151 ◽  
Author(s):  
William J. Jo ◽  
Alex Loguinov ◽  
Michelle Chang ◽  
Henri Wintz ◽  
Corey Nislow ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 888
Author(s):  
Xuejiao Jin ◽  
Jie Zhang ◽  
Tingting An ◽  
Huihui Zhao ◽  
Wenhao Fu ◽  
...  

Lithium hexafluorophosphate (LiPF6) is one of the leading electrolytes in lithium-ion batteries, and its usage has increased tremendously in the past few years. Little is known, however, about its potential environmental and biological impacts. In order to improve our understanding of the cytotoxicity of LiPF6 and the specific cellular response mechanisms to it, we performed a genome-wide screen using a yeast (Saccharomyces cerevisiae) deletion mutant collection and identified 75 gene deletion mutants that showed LiPF6 sensitivity. Among these, genes associated with mitochondria showed the most enrichment. We also found that LiPF6 is more toxic to yeast than lithium chloride (LiCl) or sodium hexafluorophosphate (NaPF6). Physiological analysis showed that a high concentration of LiPF6 caused mitochondrial damage, reactive oxygen species (ROS) accumulation, and ATP content changes. Compared with the results of previous genome-wide screening for LiCl-sensitive mutants, we found that oxidative phosphorylation-related mutants were specifically hypersensitive to LiPF6. In these deletion mutants, LiPF6 treatment resulted in higher ROS production and reduced ATP levels, suggesting that oxidative phosphorylation-related genes were important for counteracting LiPF6-induced toxicity. Taken together, our results identified genes specifically involved in LiPF6-modulated toxicity, and demonstrated that oxidative stress and ATP imbalance maybe the driving factors in governing LiPF6-induced toxicity.


2013 ◽  
Vol 63 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Naoko TAKAHASHI-ANDO ◽  
Akira TANAKA ◽  
Yohsuke SEKIMOTO ◽  
Kohta YAMAUCHI ◽  
Akinobu ECHIGO ◽  
...  

2015 ◽  
Vol 11 (11) ◽  
pp. 3129-3136 ◽  
Author(s):  
Namal V. C. Coorey ◽  
James H. Matthews ◽  
David S. Bellows ◽  
Paul H. Atkinson

Identifying Saccharomyces cerevisiae genome-wide gene deletion mutants that confer hypersensitivity to a xenobiotic aids the elucidation of its mechanism of action (MoA).


2021 ◽  
Vol 7 (9) ◽  
pp. 756
Author(s):  
Suzie Kang ◽  
Hyewon Seo ◽  
Min-Gyu Lee ◽  
Cheol-Won Yun

To understand the relationship between carbon or nitrogen utilization and iron homeostasis, we performed an iron uptake assay with several deletion mutants with partial defects in carbon or nitrogen metabolism. Among them, some deletion mutants defective in carbon metabolism partially and the MEP2 deletion mutant showed lower iron uptake activity than the wild type. Mep2 is known as a high-affinity ammonia transporter in Saccharomyces cerevisiae. Interestingly, we found that nitrogen starvation resulted in lower iron uptake activity than that of wild-type cells without downregulation of the genes involved in the high-affinity iron uptake system FET3/FTR1. However, the gene expression of FRE1 and CTR1 was downregulated by nitrogen starvation. The protein level of Ctr1 was also decreased by nitrogen starvation, and addition of copper to the nitrogen starvation medium partially restored iron uptake activity. However, the expression of MAC1, which is a copper-responsive transcriptional activator, was not downregulated by nitrogen starvation at the transcriptional level but was highly downregulated at the translational level. Mac1 was downregulated dramatically under nitrogen starvation, and treatment with MG132, which is an inhibitor of proteasome-dependent protein degradation, partially attenuated the downregulation of Mac1. Taken together, these results suggest that nitrogen starvation downregulates the high-affinity iron uptake system by degrading Mac1 in a proteasome-dependent manner and eventually downregulates copper metabolism.


1983 ◽  
Vol 80 (18) ◽  
pp. 5680-5684 ◽  
Author(s):  
D. R. Higgins ◽  
S. Prakash ◽  
P. Reynolds ◽  
R. Polakowska ◽  
S. Weber ◽  
...  

1989 ◽  
Vol 215 (3) ◽  
pp. 425-430 ◽  
Author(s):  
Francis Fabre ◽  
Nieve Magana-Schwencke ◽  
Roland Chanet

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