Causal role for jun protein in the stimulation of choline acetyltransferase by insulin in embryonic chick retina.

Previous work showed that the availability of insulin to the embryonic chick retina at a critical developmental stage stimulated the activity of the acetylcholine synthetic enzyme, choline acetyltransferase (ChAT) (R. E. Hausman et al., 1991, Dev. Brain Res. 59, 31-37). Here we show that a 2- to 5-min exposure to insulin results in a greater than 24 hr elevation in ChAT protein. Immediately following exposure to insulin there is a transient increase in the level of jun protein followed by an increase in ChAT. The stimulation of ChAT protein is not the result of an overall stimulation of protein synthesis as other proteins are not affected. Exposure of the cells to antisense oligonucleotide to jun, but not to sense oligonucleotide, reduces the increase in both jun and ChAT. These and previous results suggest that insulin is necessary for the characteristic increase in ChAT protein during retina development and that this increase requires the transient synthesis of jun.