Interactions between areas I and II direct pdx-1 expression specifically to islet cell types of the mature and developing pancreas

J Biol Chem. 2005 Nov 18;280(46):38438-44. doi: 10.1074/jbc.M508594200. Epub 2005 Sep 7.

Abstract

PDX-1 regulates transcription of genes involved in islet beta cell function and pancreas development. Islet-specific expression is controlled by 5'-flanking sequences from base pair (bp) -2917 to -1918 in transgenic experiments, which encompasses both conserved (i.e. Area I (bp -2761/-2457), Area II (bp -2153/-1923)) and non-conserved pdx-1 sequences. However, only an Area II-driven transgene is independently active in vivo, albeit in only a fraction of islet PDX-1-producing cells. Our objective was to identify the sequences within the -2917/-1918-bp region that act in conjunction with Area II to allow comprehensive expression in islet PDX-1(+) cells. In cell line-based transfection assays, only Area I effectively potentiated Area II activity. Both Area I and Area II functioned in an orientation-independent manner, whereas synergistic, enhancer-like activation was uniquely found with duplicated Area II. Chimeras of Area II and the generally active SV40 enhancer or the beta cell-specific insulin enhancer suggested that islet cell-enriched activators were necessary for Area I activation, because Area II-mediated stimulation was reduced by the SV40 enhancer and activated by the insulin enhancer. Several conserved sites within Area I were important in Area I/Area II activation, with binding at bp -2614/-2609 specifically controlled by Nkx2.2, an insulin gene regulator that is required for terminal beta cell differentiation. The ability of Area I to modulate Area II activation was also observed in vivo, as an Area I/Area II-driven transgene recapitulated the endogenous pdx-1 expression pattern in developing and adult islet cells. These results suggest that Area II is a central pdx-1 control region, whose islet cell activity is uniquely modified by Area I regulatory factors.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Base Sequence
  • Binding Sites
  • Cell Differentiation
  • Cell Line
  • Cell Nucleus / metabolism
  • Chromatin / metabolism
  • Chromatin Immunoprecipitation
  • DNA Mutational Analysis
  • Enhancer Elements, Genetic
  • Galactosides / metabolism
  • Homeobox Protein Nkx-2.2
  • Homeodomain Proteins / chemistry*
  • Homeodomain Proteins / metabolism
  • Humans
  • Immunohistochemistry
  • Indoles / metabolism
  • Insulin / genetics
  • Insulinoma / metabolism
  • Islets of Langerhans / metabolism*
  • Lac Operon
  • Mice
  • Molecular Sequence Data
  • NIH 3T3 Cells
  • Nuclear Proteins
  • Pancreas / embryology*
  • Pancreas / metabolism
  • Protein Binding
  • Protein Structure, Tertiary
  • Recombinant Fusion Proteins / chemistry
  • Trans-Activators / chemistry*
  • Trans-Activators / metabolism
  • Transcription Factors / metabolism
  • Transcription, Genetic*
  • Transfection
  • Transgenes
  • Zebrafish Proteins

Substances

  • Chromatin
  • Galactosides
  • Homeobox Protein Nkx-2.2
  • Homeodomain Proteins
  • Indoles
  • Insulin
  • NKX2-2 protein, human
  • Nkx2-2 protein, mouse
  • Nuclear Proteins
  • Recombinant Fusion Proteins
  • Trans-Activators
  • Transcription Factors
  • Zebrafish Proteins
  • nkx2.2b protein, zebrafish
  • pancreatic and duodenal homeobox 1 protein
  • 5-bromo-4-chloro-3-indolyl beta-galactoside