ArticleEukaryotic cell2008
Nonapoptotic death of Saccharomyces cerevisiae cells that is stimulated by Hsp90 and inhibited by calcineurin and Cmk2 in response to endoplasmic reticulum stresses.
Article in Eukaryotic cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- Article
- The role of plant metacaspases in cell death and survival.Cell death and differentiation · 2026Review
- The calcineurin-responsive transcription factor Crz1 regulates the expression of CMK2 via a sole CDRE site in its promoter in budding yeast.Scientific reports · 2025Article
- Calcineurin promotes adaptation to chronic stress through two distinct mechanisms.Molecular biology of the cell · 2024Article
- Calcineurin promotes adaptation to chronic stress through two distinct mechanisms.bioRxiv : the preprint server for biology · 2024Article
- Article
- Phosphate availability conditions caspofungin tolerance, capsule attachment and titan cell formation inFrontiers in fungal biology · 2024Article
- MoCbp7, a Novel Calcineurin B Subunit-Binding Protein, Is Involved in the Calcium Signaling Pathway and Regulates Fungal Development, Virulence, and ER Homeostasis inInternational journal of molecular sciences · 2023Article
- Calmodulin kinase 2 genetically interacts with Rch1p to negatively regulate calcium import into Saccharomyces cerevisiae after extracellular calcium pulse.Archives of microbiology · 2022Article
- Article
- Review
- Metabolism-induced oxidative stress and DNA damage selectively trigger genome instability in polyploid fungal cells.The EMBO journal · 2019Article
- The protein kinase Cmk2 negatively regulates the calcium/calcineurin signalling pathway and expression of calcium pump genes PMR1 and PMC1 in budding yeast.Cell communication and signaling : CCS · 2019Article
- Induction of Ptp2 and Cmp2 protein phosphatases is crucial for the adaptive response to ER stress in Saccharomyces cerevisiae.Scientific reports · 2018Article
- Ongoing resolution of duplicate gene functions shapes the diversification of a metabolic network.eLife · 2016Article
- Respiratory metabolism and calorie restriction relieve persistent endoplasmic reticulum stress induced by calcium shortage in yeast.Scientific reports · 2016Article
- A LAPF/phafin1-like protein regulates TORC1 and lysosomal membrane permeabilization in response to endoplasmic reticulum membrane stress.Molecular biology of the cell · 2015Article
- ER stress response mechanisms in the pathogenic yeast Candida glabrata and their roles in virulence.Virulence · 2014Review
- Aging and cell death in the other yeasts, Schizosaccharomyces pombe and Candida albicans.FEMS yeast research · 2014Review
- Kch1 family proteins mediate essential responses to endoplasmic reticulum stresses in the yeasts Saccharomyces cerevisiae and Candida albicans.The Journal of biological chemistry · 2013Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endoplasmic reticulum (ER) stress can trigger apoptosis and necrosis in many types of mammalian cells. Previous studies in yeast found little or no cell death in response to the ER stressor tunicamycin, but a recent study suggested widespread apoptosis-like death. Here we show that wild-type laboratory Saccharomyces cerevisiae cells responding to tunicamycin die by nonapoptotic mechanisms in low-osmolyte culture media and survive for long periods of time in standard synthetic media. Survival requires calcineurin, a Ca(2+)/calmodulin-dependent protein phosphatase, but none of its known targets. The Ca(2+)/calmodulin-dependent protein kinase Cmk2 was identified as an indirect target of calcineurin that suppresses death of calcineurin-deficient cells. Death of Cmk2- and/or calcineurin-deficient S. cerevisiae cells was preceded by accumulation of reactive oxygen species but was not associated with hallmarks of apoptosis and was not dependent on Mca1, Aif1, Nuc1, or other factors implicated in apoptosis-like death. Cmk2 and calcineurin also independently suppressed the death of S. cerevisiae cells responding to dithiothreitol or miconazole, a common azole-class antifungal drug. Though inhibitors of Hsp90 have been shown to diminish calcineurin signaling in S. cerevisiae and to synergistically inhibit growth in combination with azoles, they did not stimulate death of S. cerevisiae cells in combination with miconazole or tunicamycin, and instead they prevented the death of calcineurin- and Cmk2-deficient cells. These findings reveal a novel prodeath role for Hsp90 and antideath roles for calcineurin and Cmk2 that extend the life span of S. cerevisiae cells responding to both natural and clinical antifungal compounds.
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