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Post‐transcriptional regulation of gene expression in response to iron deficiency in S. cerevisiae
Author(s) -
Vergara Sandra Viviana,
Thiele Dennis J
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.494.6
Subject(s) - tristetraprolin , microbiology and biotechnology , iron deficiency , gene expression , gene , regulation of gene expression , messenger rna , transcriptional regulation , cellular adaptation , biology , chemistry , genetics , rna binding protein , medicine , anemia
The yeast proteins Cth1 and Cth2 belong to the Tristetraprolin (TTP) family of AU‐rich Element (ARE)‐containing mRNA‐destabilizing proteins. In response to iron (Fe)‐deficiency, Cth1 and Cth2 coordinately promote the degradation of mRNAs encoding many proteins involved in highly Fe‐dependent metabolic pathways. As a consequence, they promote a genome wide remodeling of metabolism that permits the utilization of the limited Fe in essential processes, while lowering the metabolic Fe‐demand of other non‐essential pathways. Our recent data indicate that while Cth2 expression gradually but robustly increases during Fe‐deficiency over time, Cth1 is more rapidly and only transiently expressed soon after the Fe‐deficient conditions are imposed. Furthermore, our data indicate that the CTH1 and CTH2 transcripts are themselves subject to ARE‐mediated degradation by the Cth1 and Cth2 proteins, creating an auto‐ and cross‐regulatory circuit responsible for differences in their expression. We believe that the tight regulation of Cth1 and Cth2 is a cellular strategy to adjust to either mild or transient versus severe or sustained forms of Fe‐deficiency. Our current work seeks to understand how auto‐ and cross‐regulation of Cth1 and Cth2 contributes to the cellular adaptation to Fe‐deficiency. This work is supported by NIH grant GM41840 (D.J.T) and NIH Pre‐Doctoral Fellowship 1F31‐DK081304 (S.V.V).