Cooperation of two mRNA-binding proteins drives metabolic adaptation to iron deficiency.


Journal Article

Iron (Fe) is an essential cofactor for a wide range of cellular processes. We have previously demonstrated in yeast that Cth2 is expressed during Fe deficiency and promotes degradation of a battery of mRNAs leading to reprogramming of Fe-dependent metabolism and Fe storage. We report here that the Cth2-homologous protein Cth1 is transiently expressed during Fe deprivation and participates in the response to Fe deficiency through the degradation of mRNAs primarily involved in mitochondrially localized activities including respiration and amino acid biosynthesis. In parallel, wild-type cells, but not cth1Deltacth2Delta cells, accumulate mRNAs encoding proteins that function in glucose import and storage and store high levels of glycogen. In addition, Fe deficiency leads to phosphorylation of Snf1, an AMP-activated protein kinase family member required for the cellular response to glucose starvation. These studies demonstrate a metabolic reprogramming as a consequence of Fe starvation that is dependent on the coordinated activities of two mRNA-binding proteins.

Full Text

Duke Authors

Cited Authors

  • Puig, S; Vergara, SV; Thiele, DJ

Published Date

  • June 2008

Published In

Volume / Issue

  • 7 / 6

Start / End Page

  • 555 - 564

PubMed ID

  • 18522836

Pubmed Central ID

  • 18522836

Electronic International Standard Serial Number (EISSN)

  • 1932-7420

Digital Object Identifier (DOI)

  • 10.1016/j.cmet.2008.04.010


  • eng

Conference Location

  • United States