Abstract
Although zinc deficiency evokes the endoplasmic reticulum (ER)-stress response, the activating mechanism remains obscure. Here we show that in yeast cells, the ER-stress sensor Ire1 was activated upon zinc deficiency. ER-stressing stimuli activating Ire1 are known to include ER accumulation of unfolded proteins and membrane-lipid aberrancy. According to the findings presented here, zinc deficiency causes both types of abnormality.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Biosensing Techniques
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Endoplasmic Reticulum / genetics
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Endoplasmic Reticulum / metabolism
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Endoplasmic Reticulum Stress*
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Endoribonucleases / metabolism
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Membrane Glycoproteins / genetics*
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Protein Folding
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Protein Serine-Threonine Kinases / genetics*
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Saccharomyces cerevisiae / genetics
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Saccharomyces cerevisiae / metabolism
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Saccharomyces cerevisiae Proteins / genetics*
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Signal Transduction*
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Zinc / deficiency
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Zinc / metabolism*
Substances
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Membrane Glycoproteins
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Saccharomyces cerevisiae Proteins
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IRE1 protein, S cerevisiae
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Protein Serine-Threonine Kinases
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Endoribonucleases
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Zinc