Zinc depletion activates the endoplasmic reticulum-stress sensor Ire1 via pleiotropic mechanisms

Biosci Biotechnol Biochem. 2013;77(6):1337-9. doi: 10.1271/bbb.130130. Epub 2013 Jun 7.


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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biosensing Techniques
  • Endoplasmic Reticulum / genetics
  • Endoplasmic Reticulum / metabolism
  • Endoplasmic Reticulum Stress*
  • Endoribonucleases / metabolism
  • Membrane Glycoproteins / genetics*
  • Protein Folding
  • Protein Serine-Threonine Kinases / genetics*
  • Saccharomyces cerevisiae / genetics
  • Saccharomyces cerevisiae / metabolism
  • Saccharomyces cerevisiae Proteins / genetics*
  • Signal Transduction*
  • Zinc / deficiency
  • Zinc / metabolism*


  • Membrane Glycoproteins
  • Saccharomyces cerevisiae Proteins
  • IRE1 protein, S cerevisiae
  • Protein Serine-Threonine Kinases
  • Endoribonucleases
  • Zinc