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The Saccharomyces cerevisiae Ca2+ channel Cch1pMid1p is essential for tolerance to cold stress and iron toxicity.

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The Saccharomyces cerevisiae Ca2+ channel Cch1pMid1p is essential for tolerance to cold stress and iron toxicity. / Peiter, Edgar; Fischer, Marc; Sidaway, Kate et al.
In: FEBS Letters, Vol. 579, No. 25, 24.10.2005, p. 5697-5703.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

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Peiter E, Fischer M, Sidaway K, Roberts SK, Sanders D. The Saccharomyces cerevisiae Ca2+ channel Cch1pMid1p is essential for tolerance to cold stress and iron toxicity. FEBS Letters. 2005 Oct 24;579(25):5697-5703. doi: 10.1016/j.febslet.2005.09.058

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Peiter, Edgar ; Fischer, Marc ; Sidaway, Kate et al. / The Saccharomyces cerevisiae Ca2+ channel Cch1pMid1p is essential for tolerance to cold stress and iron toxicity. In: FEBS Letters. 2005 ; Vol. 579, No. 25. pp. 5697-5703.

Bibtex

@article{86d902bb059442138e46b29aa1a5847d,
title = "The Saccharomyces cerevisiae Ca2+ channel Cch1pMid1p is essential for tolerance to cold stress and iron toxicity.",
abstract = "Cch1p and Mid1p are components of a high-affinity Ca2+-permeable channel in the yeast plasma membrane. Here, we show that growth of mutants in the Cch1pMid1p channel is markedly hypersensitive to low temperature and to high iron concentration in the medium. Both phenotypes were suppressed by high Ca2+ concentration. Iron stress elicited an increased Ca2+ influx into both wild type and cch1Δmid1Δ yeast. Inhibition of calcineurin strongly depressed growth of iron-stressed wild type yeast, indicating that calcineurin is a downstream element of the iron stress response. Iron hypersensitivity of the cch1Δmid1Δ mutant was not associated with an increased iron uptake. An involvement of oxidative stress in the iron-hypersensitive phenotype was indicated by the findings that the antioxidants tocopheryl acetate and (ethyl)glutathione improved growth and viability of the iron-stressed mutant. Further, the degree of glutathione oxidation was increased in the presence of iron. The results indicate that iron stress leads to an increased oxidative poise and that Cch1pMid1p is essential to tolerate this condition.",
keywords = "Calcium, Channel, Cold stress, Iron toxicity, Saccharomyces cerevisiae",
author = "Edgar Peiter and Marc Fischer and Kate Sidaway and Roberts, {Stephen K.} and Dale Sanders",
year = "2005",
month = oct,
day = "24",
doi = "10.1016/j.febslet.2005.09.058",
language = "English",
volume = "579",
pages = "5697--5703",
journal = "FEBS Letters",
issn = "0014-5793",
publisher = "Elsevier",
number = "25",

}

RIS

TY - JOUR

T1 - The Saccharomyces cerevisiae Ca2+ channel Cch1pMid1p is essential for tolerance to cold stress and iron toxicity.

AU - Peiter, Edgar

AU - Fischer, Marc

AU - Sidaway, Kate

AU - Roberts, Stephen K.

AU - Sanders, Dale

PY - 2005/10/24

Y1 - 2005/10/24

N2 - Cch1p and Mid1p are components of a high-affinity Ca2+-permeable channel in the yeast plasma membrane. Here, we show that growth of mutants in the Cch1pMid1p channel is markedly hypersensitive to low temperature and to high iron concentration in the medium. Both phenotypes were suppressed by high Ca2+ concentration. Iron stress elicited an increased Ca2+ influx into both wild type and cch1Δmid1Δ yeast. Inhibition of calcineurin strongly depressed growth of iron-stressed wild type yeast, indicating that calcineurin is a downstream element of the iron stress response. Iron hypersensitivity of the cch1Δmid1Δ mutant was not associated with an increased iron uptake. An involvement of oxidative stress in the iron-hypersensitive phenotype was indicated by the findings that the antioxidants tocopheryl acetate and (ethyl)glutathione improved growth and viability of the iron-stressed mutant. Further, the degree of glutathione oxidation was increased in the presence of iron. The results indicate that iron stress leads to an increased oxidative poise and that Cch1pMid1p is essential to tolerate this condition.

AB - Cch1p and Mid1p are components of a high-affinity Ca2+-permeable channel in the yeast plasma membrane. Here, we show that growth of mutants in the Cch1pMid1p channel is markedly hypersensitive to low temperature and to high iron concentration in the medium. Both phenotypes were suppressed by high Ca2+ concentration. Iron stress elicited an increased Ca2+ influx into both wild type and cch1Δmid1Δ yeast. Inhibition of calcineurin strongly depressed growth of iron-stressed wild type yeast, indicating that calcineurin is a downstream element of the iron stress response. Iron hypersensitivity of the cch1Δmid1Δ mutant was not associated with an increased iron uptake. An involvement of oxidative stress in the iron-hypersensitive phenotype was indicated by the findings that the antioxidants tocopheryl acetate and (ethyl)glutathione improved growth and viability of the iron-stressed mutant. Further, the degree of glutathione oxidation was increased in the presence of iron. The results indicate that iron stress leads to an increased oxidative poise and that Cch1pMid1p is essential to tolerate this condition.

KW - Calcium

KW - Channel

KW - Cold stress

KW - Iron toxicity

KW - Saccharomyces cerevisiae

U2 - 10.1016/j.febslet.2005.09.058

DO - 10.1016/j.febslet.2005.09.058

M3 - Journal article

VL - 579

SP - 5697

EP - 5703

JO - FEBS Letters

JF - FEBS Letters

SN - 0014-5793

IS - 25

ER -