Placental defects that impair further development of the conceptus can be due to developmental errors in particular cell lineages or to faulty vascularization in the placenta. Because the H358 mutation was lethal in early postimplantation development, any requirement for its function in later pregnancy could not be assessed in the mutant mice. The present study however, reveals that H358 is expressed in the nucleated erythroid cells of the developing chorioallantoic placenta suggesting that this protein functions in the cell population destined to establish extraembryonic he-matopoiesis. It is now important to investigate the expression of H358 in the mesodermally derived site comprising the aorta, genital ridge, and mesonephros region (AGM) of the mouse embryo. This AGM region is postulated to be the intraembryonic site of definitive hematopoietic activity in the mouse. The existence of intraembryonic sites for hematopoietic development has been shown in amphibians and birds. It will be interesting to test for the expression pattern of Hp58 at the AGM site because differences may exist in the regulation of extraembryonic hematopoi-esis and definitive hematopoiesis in which the stem cells reside in the fetal liver but may originate in the AGM.
The possibility that differential regulation involving Hp58 could occur is suggested from previous analysis of chimeric mouse conceptuses generated from two independent Hp58 mutant homozygous cell lines. There was a high level of chimerism in the fetus. However, low level or sporadic contributions were found in the extraembryonic tissues, even in chimeras where mutant cells were the predominant cell population in the embryo. Further understanding the function of Hp58 in the regulation of the extraembry-onic hematopoietic system should provide new insight into the formation and differentiation of hematopoietic cells during embryogenesis and placentation.