ArticlePloS one2011
Regulating cytoplasmic calcium homeostasis can reduce aluminum toxicity in yeast.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Aluminum Genotoxicity in Plants, Mammals, and Unicellular Eukaryotes: The Underlying Mechanisms.International journal of molecular sciences · 2026Review
- Calcium Signaling Is a Universal Carbon Source Signal Transducer and Effects an Ionic Memory of Past Carbon Sources.International journal of molecular sciences · 2025Article
- Adaptation of Proteome and Metabolism in Different Haplotypes ofMicroorganisms · 2023Article
- Expression of a Salt-Tolerant Pseudolysin in Yeast for Efficient Protein Hydrolysis under High-Salt Conditions.Biomolecules · 2022Article
- Antifungal Activity of 1,4-Dialkoxynaphthalen-2-Acyl Imidazolium Salts by Inducing Apoptosis of PathogenicPharmaceutics · 2021Article
- Article
- Glutathione depletion activates the yeast vacuolar transient receptor potential channel, Yvc1p, by reversible glutathionylation of specific cysteines.Molecular biology of the cell · 2016Article
- Altered intracellular calcium homeostasis and endoplasmic reticulum redox state in Saccharomyces cerevisiae cells lacking Grx6 glutaredoxin.Molecular biology of the cell · 2015Article
- Aluminum induces rapidly mitochondria-dependent programmed cell death in Al-sensitive peanut root tips.Botanical studies · 2014Article
- Physiological and transcriptional analysis of the effects of aluminum stress on Cryptococcus humicola.World journal of microbiology & biotechnology · 2012Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous study suggested that increased cytoplasmic calcium (Ca) signals may mediate aluminum (Al) toxicity in yeast (Saccharomyces cerevisiae). In this report, we found that a yeast mutant, pmc1, lacking the vacuolar calcium ion (Ca(2+)) pump Ca(2+)-ATPase (Pmc1p), was more sensitive to Al treatment than the wild-type strain. Overexpression of either PMC1 or an anti-apoptotic factor, such as Bcl-2, Ced-9 or PpBI-1, decreased cytoplasmic Ca(2+) levels and rescued yeast from Al sensitivity in both the wild-type and pmc1 mutant. Moreover, pretreatment with the Ca(2+) chelator BAPTA-AM sustained cytoplasmic Ca(2+) at low levels in the presence of Al, effectively making the cells more tolerant to Al exposure. Quantitative RT-PCR revealed that the expression of calmodulin (CaM) and phospholipase C (PLC), which are in the Ca(2+) signaling pathway, was down-regulated under Al stress. This effect was largely counteracted when cells overexpressed anti-apoptotic Ced-9 or were pretreated with BAPTA-AM. Taken together, our results suggest that the negative regulation of Al-induced cytoplasmic Ca signaling is a novel mechanism underlying internal resistance to Al toxicity.
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