Progressive Loss of the Spongiotrophoblast Layer of Birc6/Bruce Mutants Results in Embryonic Lethality

Genesis. 2005 Jun;42(2):91-103. doi: 10.1002/gene.20128.

Abstract

We have generated a mouse line with a mutant allele of the mouse Bruce/Birc6 gene induced by gene trap mutagenesis. Based on its structural features, Bruce is a member of the family of apoptosis inhibitor proteins (IAPs). This mutation leads to a truncated transcript and protein and results in a complete loss of the wildtype Bruce protein. Bruce mutant mice die from a progressive loss of their placental spongiotrophoblast layer between day 11.5 and 14.5 of embryonic development. The cause of the Bruce homozygous mutant phenotype is a lack of proliferation of spongiotrophoblast cells in the developing placenta. In contrast to in vitro data, which indicate a function for Bruce in apoptosis inhibition, the in vivo results presented here suggest instead a role for Bruce in cell division.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Base Sequence
  • Embryo, Mammalian / metabolism
  • Embryonic Development*
  • Gene Expression Regulation, Developmental
  • Genes, Lethal
  • Genotype
  • In Situ Hybridization
  • Inhibitor of Apoptosis Proteins
  • Mice
  • Mice, Inbred C57BL
  • Molecular Sequence Data
  • Mutagenesis
  • Neoplasm Proteins / genetics*
  • Neoplasm Proteins / physiology*
  • Phenotype
  • RNA / metabolism
  • Stem Cells / cytology
  • Trophoblasts / cytology*
  • beta-Galactosidase / genetics

Substances

  • BIRC6 protein, mouse
  • Inhibitor of Apoptosis Proteins
  • Neoplasm Proteins
  • RNA
  • beta-Galactosidase