Abstract
The transient embryonic diapause associated with delayed implantation in mice is characterized by decreases in the rates of synthesis of RNA and protein as well as a cessation of development. The present experiments were undertaken to examine the possibility that controls on protein synthesis at the level of translation of mRNA provide a regulatory mechanism in this situation. Rates of peptide chain elongation were determined in dormant embryos as well as in embryos that were reactivated either in vivo by estradiol-17 beta or by incubation in vitro. In dormant embryos the rate of peptide elongation was found to be approximately half that in active embryos. Although this change in translational efficiency appears to be sufficient to account for previously observed differences in overall rates of protein synthesis in dormant and reactivated embryos, the possibility that some changes also occur at the level of transcription during reactivation is not ruled out.
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