Estrogen receptor and the development of estrogenic responses in embryonic chick liver.

We have examined the development of responsiveness to estrogen by embryonic chick liver with a view to determining common and unique factors involved in the establishment of different genomic responses to th e hormone. The major apoproteins of chick VLDL, apo VLDL-B and apo VLDL-II, both appear to be estrogen inducible at an earlier stage of of embryonic development than is vitellogenin. Apo VLDL-B, but not vitellogenin, exhibits a significant level of hepatic synthesis in the absence of estrogen treatment. This basal synthesis in the absence of estrogen treatment. This basal synthesis is tamoxifen-resistant and is detectable at very early stages of hepatic development, well before estrogen responsiveness is seen. Immunological cross-reactivity, electrophoretic behavior and the results of limited proteolysis mapping suggest that the apo VLDL-B synthesized under basal and estrogen-stimulated conditions is the same (or a very similar) protein. Inducibility of the VLDL apoproteins appears to parallel the appearance of the hepatic estrogen receptor system at days 10-12 while vitellogenin induction is delayed by several days. Cytosol receptor concentration undergoes a gradual increase up to the 19th day of development and thereafter declines. The properties of the 19-day receptor are very similar to those of cytosol receptor in hatched chickens, but the fall in concentration does not appear to be proportionately related to inducibility of estrogenic responses, as measured by the relative rates of synthesis in vitro.