Crim1 is required for normal junctional zone development of the murine placenta

Abstract

We are currently investigating the role of Crim1, a type-1 transmembrane protein, in placenta development using a gene-trap line, KST264. Mice homozygous for Crim1 die perinatally and display abnormalities including syndactlyly of the digits, eye defects, hematomas, skin blebbing, as well as defects in the extra-embryonic tissue, the placenta. In the developing murine placenta, Crim1 is expressed in the spongiotrophoblasts of the junctional zone layer, in the trophoblast giant cells and in the arterial vascular network. In the Crim1 KST264/ KST264 the placental phenotype is apparent by E15.5 where by gross morphology the placenta appears to have a smaller junctional zone layer. At E17.5, the homozygous placentae are smaller compared to age-matched wild-type placentae (p= <0.01). Early investigations reveal that there are no gross vascular defects in the Crim1 KST264/ KST264, however in situ analysis of 4311 (tpbp), a marker of spongiotrophoblasts and glycogen cells, shows that there is a structural defect in the formation of the junctional zone. We are investigating whether this is due to abnormal differentiation, proliferation rates or migration of cellular subtypes within the junctional zone. (This research is supported by NHMRC grant # 455972. GK is supported by an Australian Postgraduate Award)