This chapter outlines the clocks of genome activation from the early stage of mobile Ca2+ fluxes in the sperm eliciting stable Ca2+ currents in the fertilized egg through polarization for the mitotic and postmitotic events creating the apical domain. This chapter also emphasizes the role of clock genes in dictating the times of molecule allocation for protection of the mitochondria resulting from their very early ultradian oscillations, their modulatory interplay with Ca2+ currents, their effects on transcriptomic processes of other genes, and their capacity to activate electron transporters for the conversion of unstable molecules to stable ones. The chapter integrates recent data on the design of clock genes as shown in the impact of their ultradian oscillations on chromatin, RohA, and F-actin and their enzymatic cascades, which are the early molecular events for apical domain enrichment and the inner cell population of embryonic development. The chapter continues showing the pathways developing from the early molecular processes of genome activation through the birth of the first neuron, the formation of the neural tube, and its closure. As such, this chapter emphasizes the crucial early role of clock genes in leading towards neural developmental progression before their shift to circadian rhythms upon the maturation of the suprachiasmatic nucleus at mid-gestation. It is concluded that the molecular ultradian oscillations of clock genes during embryonic phases result in time-specific electrical fields when they interact with Ca2+ currents. As such, clock genes turn to be an originating source for elicitation, followed by suppression periods, of stereotyped short behavioral cycles, typical in embryos before the gestational timing of the neural tube closure.