Following exposure of the parental female to high temperature approximately 40 percent of the embryos are arrested at the two-cell stage and fail to incorporate [³H] uridine. An additional 20 percent of the two-cell embryos are only partially affected in that one blastomere is able to undergo a limited number of cleavage divisions. The ‘cleaving’ blastomeres of these embryos demonstrate a distribution of isotope comparable to the blastomeres of normal embryos at the same chronological stages of dvelopment. In contrast, the incorporation of isotope into the ‘arrested’ blastomere, if it occurs, is confined to the nucleus and never assumes the pattern typical of blastomeres at later stages of development.

Paternal hyperthermia, an effect conveyed by the fertilizing spermatozoan, allows normal embryonic development during the early cleavage stages. However, the rate of development is retarded at the morula stage although blastulation eventually occurs. A significant proportion of embryos at the 8-cell and morula stages also contain blastomeres which fail to incorporate the isotopic precursor. Consequently, the retardation in embryonic development is preceded by a partial failure to synthesize RNA. These embryos are considered to be responsible for the embryonic mortality that is known to occur at, or shortly after, implantation.