Dividing liver cells, fibroblasts, or Hela cells generally yield daughters with the genetic program of the mother cell. I have termed such cell cycles "proliferative." During embryogenesis there are cell cycles that yield progeny with genetic programs differing from that of the mother cell. These cell cycles I have termed "quantal". I propose that a small number of quantal cell cycles, alternating with variable numbers of proliferative cycles are obligatory to the step-wise events producing a cell with the machinery to translate molecules like myosin or hemoglobin. The mother of the myoblast is the presumptive myoblast and it does not synthesize skeletal myosin. The mother of the primitive erythroblast is the hematocytoblast and it does not synthesize hemoglobin. I propose that there is a DNA- dependent, or cell cycle- dependent event that is required for this genetic reprogramming of daughter cells. This view relegates "embryonic induction" to (1) mitotic stimulators, or, (2) hormone-like agents only acting on genetically primed cells. This view stresses that the major genetic decisions were made long before the myoblast synthesizes its first molecule of myosin, or the erythroblast of hemoglobin. The genetic decisions were made in part in the mother and in part in earlier ancestral cells. More must be learned about cytoplasmic-nuclear mechanisms accounting for transmissibility and change emerging in cell lineages. To these ends the effect of BudR on differentiating cells will be probed. Isotopes will be used to monitor the pertinent proteins, polysaccharides, and RNAs. Fluorescein-labelled antibodies will be used when examining "mixed" cell populations. Electron microscopy will also be used.