Arsenic-induced alterations in embryonic transcription factor gene expression: Implications for abnormal neural development

B. Wlodarczyk, G. D. Bennett, James Arthur Calvin, J. C. Craig, R. H. Finnell*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

35 Scopus citations

Abstract

We examined the morphological and molecular consequences of acute in utero exposure to teratogenic concentrations of arsenate. The treatment produced a dose-related increase in neural tube defects, along with a significant alteration in the pattern of gene expression for several transcription factors (creb, Hox 3.1, Pax3, and Emx-1) that were examined using in situ transcription and antisense RNA amplification procedures. On gestational day 9:0, there was a significant delay in the embryos progression through neural tube closure, accompanied by a significant downregulation of Hox 3.1 expression and a significant upregulation of Pax3, Emx-1, and creb. As both Hox 3.1 and Pax3 serve to regulate N-CAM expression, it is possible that abnormalities associated with N-CAM may compromise neural crest cell migration and normal neural tube closure.

Original languageEnglish (US)
Pages (from-to)306-315
Number of pages10
JournalDevelopmental Genetics
Volume18
Issue number4
DOIs
StatePublished - Jul 30 1996

Keywords

  • Transcription factors
  • arsenic
  • birth defects
  • gene expression
  • murine embryos
  • neural tube defects

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology
  • Cell Biology

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