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Transcriptional response of Saccharomyces cerevisiae to potassium starvation

BACKGROUND: Ion homeostasis is essential for every cell and aberrant cation homeostasis is related to diseases like Alzheimer’s disease and epilepsy. The mechanisms responsible for cation homeostasis are only partly understood. The yeast Saccharomyces cerevisiae is an excellent organism to study fun...

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Autores principales: Anemaet, Ida G, van Heusden, G Paul H
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289377/
https://www.ncbi.nlm.nih.gov/pubmed/25432801
http://dx.doi.org/10.1186/1471-2164-15-1040
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author Anemaet, Ida G
van Heusden, G Paul H
author_facet Anemaet, Ida G
van Heusden, G Paul H
author_sort Anemaet, Ida G
collection PubMed
description BACKGROUND: Ion homeostasis is essential for every cell and aberrant cation homeostasis is related to diseases like Alzheimer’s disease and epilepsy. The mechanisms responsible for cation homeostasis are only partly understood. The yeast Saccharomyces cerevisiae is an excellent organism to study fundamental aspects of cation homeostasis. In this study we investigated the transcriptional response of this yeast to potassium starvation by using Serial Analysis of Gene Expression (SAGE)-tag sequencing. RESULTS: Comparison of transcript levels in cells grown for 60 min in media without potassium with those in cells grown under standard potassium concentrations showed that the mRNA levels of 105 genes were significantly (P < 0.01) up-regulated more than 2.0-fold during potassium starvation and the mRNA levels of 172 genes significantly down-regulated. These genes belong to several functional categories. Genes involved in stress response including HSP30, YRO2 and TPO2 and phosphate metabolism including PHO84, PHO5 and SPL2 were highly up-regulated. Analysis of the promoter of PHO84 encoding a high affinity phosphate transporter, revealed that increased PHO84 RNA levels are caused by both increased Pho4-dependent transcription and decreased RNA turnover. In the latter process antisense transcription may be involved. Many genes involved in cell cycle control, and to a lesser extent genes involved in amino acid transport, were strongly down-regulated. CONCLUSIONS: Our study showed that yeast cells respond to potassium starvation in a complex way and reveals a direct link between potassium homeostasis and phosphate metabolism. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1471-2164-15-1040) contains supplementary material, which is available to authorized users.
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spelling pubmed-42893772015-01-11 Transcriptional response of Saccharomyces cerevisiae to potassium starvation Anemaet, Ida G van Heusden, G Paul H BMC Genomics Research Article BACKGROUND: Ion homeostasis is essential for every cell and aberrant cation homeostasis is related to diseases like Alzheimer’s disease and epilepsy. The mechanisms responsible for cation homeostasis are only partly understood. The yeast Saccharomyces cerevisiae is an excellent organism to study fundamental aspects of cation homeostasis. In this study we investigated the transcriptional response of this yeast to potassium starvation by using Serial Analysis of Gene Expression (SAGE)-tag sequencing. RESULTS: Comparison of transcript levels in cells grown for 60 min in media without potassium with those in cells grown under standard potassium concentrations showed that the mRNA levels of 105 genes were significantly (P < 0.01) up-regulated more than 2.0-fold during potassium starvation and the mRNA levels of 172 genes significantly down-regulated. These genes belong to several functional categories. Genes involved in stress response including HSP30, YRO2 and TPO2 and phosphate metabolism including PHO84, PHO5 and SPL2 were highly up-regulated. Analysis of the promoter of PHO84 encoding a high affinity phosphate transporter, revealed that increased PHO84 RNA levels are caused by both increased Pho4-dependent transcription and decreased RNA turnover. In the latter process antisense transcription may be involved. Many genes involved in cell cycle control, and to a lesser extent genes involved in amino acid transport, were strongly down-regulated. CONCLUSIONS: Our study showed that yeast cells respond to potassium starvation in a complex way and reveals a direct link between potassium homeostasis and phosphate metabolism. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1471-2164-15-1040) contains supplementary material, which is available to authorized users. BioMed Central 2014-11-29 /pmc/articles/PMC4289377/ /pubmed/25432801 http://dx.doi.org/10.1186/1471-2164-15-1040 Text en © Anemaet and van Heusden; licensee BioMed Central. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Anemaet, Ida G
van Heusden, G Paul H
Transcriptional response of Saccharomyces cerevisiae to potassium starvation
title Transcriptional response of Saccharomyces cerevisiae to potassium starvation
title_full Transcriptional response of Saccharomyces cerevisiae to potassium starvation
title_fullStr Transcriptional response of Saccharomyces cerevisiae to potassium starvation
title_full_unstemmed Transcriptional response of Saccharomyces cerevisiae to potassium starvation
title_short Transcriptional response of Saccharomyces cerevisiae to potassium starvation
title_sort transcriptional response of saccharomyces cerevisiae to potassium starvation
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289377/
https://www.ncbi.nlm.nih.gov/pubmed/25432801
http://dx.doi.org/10.1186/1471-2164-15-1040
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