Zinc Depletion Activates the Endoplasmic Reticulum-Stress Sensor Ire1 via Pleiotropic Mechanisms

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 unfol...

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Bibliographic Details
Published in:Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2013, Vol.77 (6), p.1337-1339
Main Authors: NGUYEN, Thanh Sy Le, KOHNO, Kenji, KIMATA, Yukio
Format: Article
Language:English
Subjects:
Biosensing Techniques
Endoplasmic Reticulum - genetics
Endoplasmic Reticulum - metabolism
Endoplasmic Reticulum Stress
Endoribonucleases - metabolism
Membrane Glycoproteins - genetics
mineral
organelle
Protein Folding
Protein-Serine-Threonine Kinases - genetics
Saccharomyces cerevisiae
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae - metabolism
Saccharomyces cerevisiae Proteins - genetics
Signal Transduction
stress response
trace element
Zinc - deficiency
Zinc - metabolism
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Summary: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.
ISSN:0916-8451
1347-6947
DOI:10.1271/bbb.130130