Characterization of Notch3-deficient mice: normal embryonic development and absence of genetic interactions with a Notch1 mutation

Genesis. 2003 Nov;37(3):139-43. doi: 10.1002/gene.10241.

Abstract

The Notch signaling pathway is an evolutionarily conserved signaling mechanism and mutations in its components disrupt cell fate specification and embryonic development in many organisms. To analyze the in vivo role of the Notch3 gene in mice, we created a deletion allele by gene targeting. Embryos homozygous for this mutation developed normally and homozygous mutant adults were viable and fertile. We also examined whether we could detect genetic interactions during early embryogenesis between the Notch3 mutation and a targeted mutation of the Notch1 gene. Double homozygous mutant embryos exhibited defects normally observed in Notch1-deficient embryos, but we detected no obvious synergistic effects in the double mutants. These data demonstrate that the Notch3 gene is not essential for embryonic development or fertility in mice, and does not have a redundant function with the Notch1 gene during early embryogenesis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Embryonic and Fetal Development / genetics*
  • Female
  • Fertility / genetics
  • Gene Deletion*
  • Gene Expression Regulation, Developmental*
  • Genetic Vectors
  • Male
  • Mice / embryology
  • Mutation
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins / pharmacology*
  • Receptor, Notch1
  • Receptor, Notch3
  • Receptor, Notch4
  • Receptors, Cell Surface / genetics*
  • Receptors, Cell Surface / physiology
  • Receptors, Notch
  • Signal Transduction
  • Transcription Factors*

Substances

  • Notch1 protein, mouse
  • Notch3 protein, mouse
  • Proto-Oncogene Proteins
  • Receptor, Notch1
  • Receptor, Notch3
  • Receptor, Notch4
  • Receptors, Cell Surface
  • Receptors, Notch
  • Transcription Factors
  • Notch4 protein, mouse