The effects of actinomycin D on the early development of quail and chick embryos
In agreement with previous work it has been found that treatment of chick embryos at an early stage of development with small concentrations of actinomycin D (2·0–4·0 × 10−8m) produces abnormalities of the brain, neural tube and somites but allows near normal development of heart and blood islands. Similar effects are produced on quail embryos by even smaller concentrations of actinomycin D (0·8–1·0 × 10−8m). In addition to the effect on the embryo, actinomycin D severely restricts the outgrowth of the explanted blastoderm; an effect which becomes obvious after about 8 h culture and coincides with the detachment of the blastoderm edge from the supporting vitelline membrane. Histological examination of the edge of the blastoderm shows that many cells have been killed by the actinomycin D. The pronounced effect of actinomycin D on the growth of the blastoderm cannot be ignored as a factor which causes the embryos to develop abnormally and it is suggested that it may even be the primary cause of the abnormalities. Under these circumstances any interpretation of the effects produced in the embryos in terms of the selective inhibition, or lack of inhibition, of specific messenger RNAs by actinomycin D seems to be unwarranted. Using [3H]actinomycin D an estimate has been made of the concentration of the compound in the blastoderm tissues at the time when the embryonic abnormalities are produced. The total DNA content of the blastoderms has also been determined. These measurements indicate that the ratio between actinomycin D molecules and guanosine residues in the treated tissue is very low (of the order of 1:20000) and would probably not allow an effective inhibition of DNA-dependent RNA synthesis.