ArticleThe Journal of biological chemistry2013
Kch1 family proteins mediate essential responses to endoplasmic reticulum stresses in the yeasts Saccharomyces cerevisiae and Candida albicans.
Article in The Journal of biological chemistry, 2013. 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, 18 citations in OpenAlex.
- Echinocandin tolerance and persistencemBio · 2026Article
- Review
- Modeling Calcium Signaling inFrontiers in molecular biosciences · 2022Article
- CaGdt1 plays a compensatory role for the calcium pump CaPmr1 in the regulation of calcium signaling and cell wall integrity signaling in Candida albicans.Cell communication and signaling : CCS · 2018Article
- Antifungal tolerance is a subpopulation effect distinct from resistance and is associated with persistent candidemia.Nature communications · 2018Article
- HG3 (Bethesda, Md.) · 2017Article
- Identification of Genes in Candida glabrata Conferring Altered Responses to Caspofungin, a Cell Wall Synthesis Inhibitor.G3 (Bethesda, Md.) · 2016Article
- The antifungal plant defensin AtPDF2.3 from Arabidopsis thaliana blocks potassium channels.Scientific reports · 2016Article
- Palmitoylation of the Cysteine Residue in the DHHC Motif of a Palmitoyl Transferase Mediates Ca2+ Homeostasis in Aspergillus.PLoS genetics · 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
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The activation of a high affinity Ca(2+) influx system (HACS) in the plasma membrane is required for survival of yeast cells exposed to natural or synthetic inhibitors of essential processes (secretory protein folding or sterol biosynthesis) in the endoplasmic reticulum (ER). The mechanisms linking ER stress to HACS activation are not known. Here we show that Kch1, a recently identified low affinity K(+) transporter in the plasma membrane of Saccharomyces cerevisiae, is up-regulated in response to several ER stressors and necessary for HACS activation. The activation of HACS required extracellular K(+) and was also dependent on the high affinity K(+) transporters Trk1 and Trk2. However, a paralog of Kch1 termed Kch2 was not expressed and not necessary for HACS activation in these conditions. The pathogenic yeast Candida albicans carries only one homolog of Kch1/Kch2, and homozygous knock-out mutants were similarly deficient in the activation of HACS during the responses to tunicamycin. However, the Kch1 homolog was not necessary for HACS activation or cell survival in response to several clinical antifungals (azoles, allylamines, echinocandins) that target the ER or cell wall. Thus, Kch1 family proteins represent a conserved linkage between HACS and only certain classes of ER stress in these yeasts.
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