The data reported here indicate that the expression of a protein with sequence similarity to H358 is spatially and temporally regulated during the formation and maturation of the chorioallantoic placenta in the rat. During pregnancy, H358 is differentially expressed in the maternal endometrium, decidua, and fetal placental cells. The H358 in the fetal placenta was regulated temporally and in a cell-specific fashion. During the early development of the chorioallantoic placenta at Day 10 of pregnancy, H358 expression was evident in nucleated fetal erythroid cells within the developing vasculature located in the chorioallantoic pri-mordia. Nucleated erythroid cells continued to express H358 throughout chorioallantoic placental maturation (Days 10-14). At Day 14 of pregnancy, expression of H358 expanded into other cell types including the trophoblast giant cells and the syncytiotrophoblast of the labyrinth region of the placenta. Taken together, our data suggest that H358 may function in both maternal and fetal tissues during the formation and maturation of the chorioallantoic placenta. Importantly, the distribution of H358 in fetal erythroid stem cells raises important implications for this protein as a participant in the regulatory networks involved in hematopoietic development.
Previous studies showed that mutation of the H358 gene in the mouse caused embryonic death shortly after implantation. Development proceeded until the primitive streak stage when abnormalities in the embryonic ectoderm, amnion, and chorion were detected. Although H358 was expressed in the oocyte and early embryo, the lack of the gene product did not inhibit preimplantation development or the ability of embryos to implant. Instead there was a failure of the chorion and allantois to fuse and form the chorioallantoic placenta. To ensure developmental success, an extensive and intimate relationship between the mother and conceptus develops in eutherian mammals. Mice lacking the H358 gene product presumably die because the embryo is completely dependent on the maternal vasculature for its source of nutrients, gas exchange, and elimination of toxic wastes. Failure to establish and maintain vascular circulation, exemplified by the H358 mutation, and lack of transition from yolk-sac-based to liver-based hematopoiesis are lethal events in eutherian mammals.