Vezf1 regulates genomic DNA methylation through its effects on expression of DNA methyltransferase Dnmt3b. Academic Article uri icon

Overview

MeSH

  • Animals
  • Cell Line
  • Embryo, Mammalian
  • Embryonic Stem Cells
  • Gene Deletion
  • Mice
  • Transfection

MeSH Major

  • DNA (Cytosine-5-)-Methyltransferase
  • DNA Methylation
  • Gene Expression Regulation, Developmental
  • Kruppel-Like Transcription Factors

abstract

  • The zinc finger protein vascular endothelial zinc finger 1 (Vezf1) has been implicated in the development of the blood vascular and lymphatic system in mice, and has been characterized as a transcriptional activator in some systems. The chicken homolog, BGP1, has binding sites in the beta-globin locus, including the upstream insulator element. We report that in a mouse embryonic stem cell line deletion of both copies of Vezf1 results in loss of DNA methylation at widespread sites in the genome, including Line1 elements and minor satellite repeats, some imprinted genes, and several CpG islands. Loss of methylation appears to arise from a substantial decrease in the abundance of the de novo DNA methyltransferase, Dnmt3b. These results suggest that naturally occurring mutations in Vezf1/BGP1 might have widespread effects on DNA methylation patterns and therefore on epigenetic regulation of gene expression.

publication date

  • August 1, 2008

has subject area

  • Animals
  • Cell Line
  • DNA (Cytosine-5-)-Methyltransferase
  • DNA Methylation
  • Embryo, Mammalian
  • Embryonic Stem Cells
  • Gene Deletion
  • Gene Expression Regulation, Developmental
  • Kruppel-Like Transcription Factors
  • Mice
  • Transfection

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2492749

Digital Object Identifier (DOI)

  • 10.1101/gad.1658408

PubMed ID

  • 18676812

Additional Document Info

start page

  • 2075

end page

  • 2084

volume

  • 22

number

  • 15