An iron enhancer element in the FTN-1 gene directs iron-dependent expression in Caenorhabditis elegans intestine

J Biol Chem. 2008 Jan 11;283(2):716-25. doi: 10.1074/jbc.M707043200. Epub 2007 Nov 16.

Abstract

Ferritin is a ubiquitous protein that sequesters iron and protects cells from iron toxicity. Caenorhabditis elegans express two ferritins, FTN-1 and FTN-2, which are transcriptionally regulated by iron. To identify the cis-acting sequences and proteins required for iron-dependent regulation of ftn-1 and ftn-2 expression, we generated transcriptional GFP reporters corresponding to 5 '-upstream sequences of the ftn-1 and ftn-2 genes. We identified a conserved 63-bp sequence, the iron-dependent element (IDE), that is required for iron-dependent regulation of a ftn-1 GFP reporter in intestine. The IDE contains two GATA-binding motifs and three octameric direct repeats. Site-directed mutagenesis of the GATA sequences, singly or in combination, reduces ftn-1 GFP reporter expression in the intestine. In vitro DNA mobility shift assays show that the intestine-specific GATA protein ELT-2 binds to both GATA sequences. Inhibition of ELT-2 function by RNA interference blocks ftn-1 GFP reporter expression in vivo. Insertion of the IDE into the promoter region of a heterologous reporter activates iron-dependent transcription in intestine. These data demonstrate that the activation of ftn-1 and ftn-2 transcription by iron requires ELT-2 and that the IDE functions as an iron-dependent enhancer in intestine.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Base Sequence
  • Caenorhabditis / genetics
  • Caenorhabditis elegans / genetics*
  • Caenorhabditis elegans / growth & development
  • Conserved Sequence
  • Digestive System Physiological Phenomena
  • Enhancer Elements, Genetic*
  • Ferritins / genetics*
  • Gene Expression Regulation / drug effects*
  • Genes, Reporter
  • Genotype
  • Intestines / physiology*
  • Iron / pharmacology*
  • Molecular Sequence Data
  • Protein Isoforms / genetics
  • RNA, Messenger / drug effects
  • RNA, Messenger / genetics

Substances

  • Protein Isoforms
  • RNA, Messenger
  • Ferritins
  • Iron