The placenta is essential for fetal growth because it promotes the delivery
of nutrients and oxygen from the maternal circulation. In mice, many gene
mutations disrupt formation of the placenta, with specific effects at diffe
rent times and on different components. Studies of these mutations are begi
nning to provide insights into both the molecular pathways required for for
mation of different placental substructures and the nature of intercellular
interactions, between trophoblast, mesenchymal and vascular components, th
at regulate placental development. Conserved gene expression patterns in hu
mans should enable the elucidation of the molecular basis of human placenta
l dysfunction.