Cch1p mediates Ca2+ influx to protect Saccharomyces cerevisiae against eugenol toxicity.

Eugenol has antifungal activity and is recognised as having therapeutic potential. However, little is known of the cellular basis of its antifungal activity and a better understanding of eugenol tolerance should lead to better exploitation of eugenol in antifungal therapies. The model yeast, Sacchar...

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Autores principales:	Stephen K Roberts, Martin McAinsh, Lisa Widdicks
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/787d9c73dbb444b78f0b9b3d405359dd
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spelling	oai:doaj.org-article:787d9c73dbb444b78f0b9b3d405359dd2021-11-18T07:05:44ZCch1p mediates Ca2+ influx to protect Saccharomyces cerevisiae against eugenol toxicity.1932-620310.1371/journal.pone.0043989https://doaj.org/article/787d9c73dbb444b78f0b9b3d405359dd2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028482/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Eugenol has antifungal activity and is recognised as having therapeutic potential. However, little is known of the cellular basis of its antifungal activity and a better understanding of eugenol tolerance should lead to better exploitation of eugenol in antifungal therapies. The model yeast, Saccharomyces cerevisiae, expressing apoaequorin was used to show that eugenol induces cytosolic Ca(2+) elevations. We investigated the eugenol Ca(2+) signature in further detail and show that exponentially growing cells exhibit Ca(2+) elevation resulting exclusively from the influx of Ca(2+) across the plasma membrane whereas in stationary growth phase cells Ca(2+) influx from intracellular and extracellular sources contribute to the eugenol-induced Ca(2+) elevation. Ca(2+) channel deletion yeast mutants were used to identify the pathways mediating Ca(2+) influx; intracellular Ca(2+) release was mediated by the vacuolar Ca(2+) channel, Yvc1p, whereas the Ca(2+) influx across the plasma membrane could be resolved into Cch1p-dependent and Cch1p-independent pathways. We show that the growth of yeast devoid the plasma membrane Ca(2+) channel, Cch1p, was hypersensitive to eugenol and that this correlated with reduced Ca(2+) elevations. Taken together, these results indicate that a cch1p-mediated Ca(2+) influx is part of an intracellular signal which protects against eugenol toxicity. This study provides fresh insight into the mechanisms employed by fungi to tolerate eugenol toxicity which should lead to better exploitation of eugenol in antifungal therapies.Stephen K RobertsMartin McAinshLisa WiddicksPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 9, p e43989 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Stephen K Roberts Martin McAinsh Lisa Widdicks Cch1p mediates Ca2+ influx to protect Saccharomyces cerevisiae against eugenol toxicity.
description	Eugenol has antifungal activity and is recognised as having therapeutic potential. However, little is known of the cellular basis of its antifungal activity and a better understanding of eugenol tolerance should lead to better exploitation of eugenol in antifungal therapies. The model yeast, Saccharomyces cerevisiae, expressing apoaequorin was used to show that eugenol induces cytosolic Ca(2+) elevations. We investigated the eugenol Ca(2+) signature in further detail and show that exponentially growing cells exhibit Ca(2+) elevation resulting exclusively from the influx of Ca(2+) across the plasma membrane whereas in stationary growth phase cells Ca(2+) influx from intracellular and extracellular sources contribute to the eugenol-induced Ca(2+) elevation. Ca(2+) channel deletion yeast mutants were used to identify the pathways mediating Ca(2+) influx; intracellular Ca(2+) release was mediated by the vacuolar Ca(2+) channel, Yvc1p, whereas the Ca(2+) influx across the plasma membrane could be resolved into Cch1p-dependent and Cch1p-independent pathways. We show that the growth of yeast devoid the plasma membrane Ca(2+) channel, Cch1p, was hypersensitive to eugenol and that this correlated with reduced Ca(2+) elevations. Taken together, these results indicate that a cch1p-mediated Ca(2+) influx is part of an intracellular signal which protects against eugenol toxicity. This study provides fresh insight into the mechanisms employed by fungi to tolerate eugenol toxicity which should lead to better exploitation of eugenol in antifungal therapies.
format	article
author	Stephen K Roberts Martin McAinsh Lisa Widdicks
author_facet	Stephen K Roberts Martin McAinsh Lisa Widdicks
author_sort	Stephen K Roberts
title	Cch1p mediates Ca2+ influx to protect Saccharomyces cerevisiae against eugenol toxicity.
title_short	Cch1p mediates Ca2+ influx to protect Saccharomyces cerevisiae against eugenol toxicity.
title_full	Cch1p mediates Ca2+ influx to protect Saccharomyces cerevisiae against eugenol toxicity.
title_fullStr	Cch1p mediates Ca2+ influx to protect Saccharomyces cerevisiae against eugenol toxicity.
title_full_unstemmed	Cch1p mediates Ca2+ influx to protect Saccharomyces cerevisiae against eugenol toxicity.
title_sort	cch1p mediates ca2+ influx to protect saccharomyces cerevisiae against eugenol toxicity.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/787d9c73dbb444b78f0b9b3d405359dd
work_keys_str_mv	AT stephenkroberts cch1pmediatesca2influxtoprotectsaccharomycescerevisiaeagainsteugenoltoxicity AT martinmcainsh cch1pmediatesca2influxtoprotectsaccharomycescerevisiaeagainsteugenoltoxicity AT lisawiddicks cch1pmediatesca2influxtoprotectsaccharomycescerevisiaeagainsteugenoltoxicity
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Cch1p mediates Ca2+ influx to protect Saccharomyces cerevisiae against eugenol toxicity.

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