Cell proliferation patterns during cytodifferentiation in embryonic chick tissues: liver, heart and erythrocytes.

Tritiated thymidine was administered to four groups of embryos at various stages of development. The first group was killed 45 min after isotope administration. The second group received the isotope three times over a 12 h period, the third group four times over a 24 h period, and the last group eight times over a 48 h period. Sagittal histological sections of the embryos were prepared for radioautography. In the radioautographs the percentage labeled nuclei were scored as an index of cell proliferation. The following observations were made. From stage 10 to 23 (45 min series) there is a progressive increase in the proliferative index of the labeled erythrocytes. This was followed by a precipitous drop as embryonic age increased. At stage 23 of the .12 h series, 97% of the cells were labeled. The 24 and 48 h series of embryos also exhibit a high labeling index, 97% and 95% respectively, by stages 20-24. This indicates that at these stages most of the cells were in the proliferative pool. In correlation with the demonstrated presence of hemoglobin as early as stage 10, it was concluded that cell proliferation and cytodifferentiation in chick primary erythrocytes are not mutually exclusive. A random pattern of proliferative activity existed in the liver of the early embryos; however, at stage 29 the periphery began to show a higher labeling index than was found in the center. This indicates that liver growth was primarily appositional. From stage 29 through hatching there was a gradual decline in the labeling index. After hatching a burst of proliferative activity occurred but the appositional pattern of growth was not seen. The proliferative activity of the littoral cells remained relatively constant when compared to that of the hepatic parenchymal cells. This suggests that the control of their proliferative activity was somewhat different from that of the hepatic parenchymal cells. The relationship of cell proliferation and cytodifferentiation in the liver could not be established. There was a progressive increase in the proliferative index of the heart ventricular myoblasts from stage 12 through stage 20-23. This was followed by a gradual decline in proliferation as embryonic age increased. An appositional growth of the heart was also demonstrated. Cytodifferentiation of heart myoblasts is known to occur as early as stage 10. Almost all of the myoblasts were labeled at stages 32 and 33 of the group exposed to the isotope for 48 h. This indicates that, in the heart, cytodifferentiation and cell proliferation are not mutually exclusive processes.