Proliferative defect and embryonic lethality in mice homozygous for a deletion in the p110alpha subunit of phosphoinositide 3-kinase

J Biol Chem. 1999 Apr 16;274(16):10963-8. doi: 10.1074/jbc.274.16.10963.

Abstract

Phosphatidylinositol 3,4,5-trisphosphate is a phospholipid signaling molecule involved in many cellular functions including growth factor receptor signaling, cytoskeletal organization, chemotaxis, apoptosis, and protein trafficking. Phosphorylation at the 3 position of the inositol ring is catalyzed by many different 3-kinases (classified as types IA, IB, II, and III), but the physiological roles played by each of the different 3-kinase isozymes during embryonic development and in homeostasis in animals is incompletely understood. Mammalian type IA kinase isozymes are heterodimers that are active at 37 degrees C when the catalytic 110-kDa subunit interacts through an amino-terminal binding domain with a regulatory 85- or 55-kDa subunit. Using gene targeting in embryonic stem cells, we deleted this binding domain in the gene encoding the alpha isoform of the 110-kDa catalytic subunit (Pik3ca) of the alpha isozyme of the type IA kinases, leading to loss of expression of the p110 catalytic subunit. We show that Pik3cadel/del embryos are developmentally delayed at embryonic day (E) 9.5 and die between E9.5 and E10.5. E9. 5 Pik3cadel/del embryos have a profound proliferative defect but no increase in apoptosis. A proliferative defect is supported by the observation that fibroblasts from Pik3cadel/del embryos fail to replicate in Dulbecco's modified Eagle's medium and fetal calf serum, even with supplemental growth factors.

MeSH terms

  • Animals
  • Base Sequence
  • Blotting, Western
  • Cell Division / genetics*
  • Chromosome Mapping
  • Cloning, Molecular
  • DNA Primers
  • Embryo, Mammalian / cytology
  • Gene Targeting
  • Genes, Lethal*
  • Genetic Vectors
  • Homozygote*
  • In Situ Nick-End Labeling
  • Mice
  • Phenotype
  • Phosphatidylinositol 3-Kinases / genetics*
  • RNA, Messenger / genetics
  • Sequence Deletion*

Substances

  • DNA Primers
  • RNA, Messenger
  • Phosphatidylinositol 3-Kinases