Out of 199 weanlings from heterozygous intercrosses, no Capn2-/- progeny were detected (Table 2). We did not observe high rates of perinatal death, and no Capn2-/- stillborns were observed. This suggested that Capn2-/- animals perished at some stage during embryonic development. In an attempt to determine if embryonic death occurred at a post-implantation stage, embryos were harvested for genotyping at different times between E10.5 and E18.5. No Capn2-/- embryos were observed and no signs of embryo resorption were detected (Table 2). This indicated that the Capn2-/- embryos might be dying prior to implantation. Embryos were then flushed from the oviducts of pregnant females at E2.5 or E3.5, and genotyped by means of a nested PCR strategy (Figure 4). Two of 90 successfully genotyped pre-implantation embryos were Capn2-/-, (Table 2; Figure 5). Both of these Capn2-/- embryos were isolated at the 8-cell stage and did not display any obvious morphological defects. None of the 46 successfully genotyped blastocyst-staged embryos were Capn2-/-. The scarcity of Capn2-deficient embryos surviving to the 8-cell stage suggested that the loss of m-calpain activity must fatally compromise the viability of early embryos. Furthermore, it is possible that persistence of some maternally derived mRNA transcript or protein might have allowed a small number of Capn2-/- embryos to survive to the morula-stage.