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 activit y of the acetylcholine synthetic enzyme, choline acetyltransferase (Ch AT) (R. E. Hausman et al., 1991, Dev. Brain Res. 59, 31-37). Here we s how that a 2- to 5-min exposure to insulin results in a greater than 2 4 hr elevation in ChAT protein. Immediately following exposure to insu lin 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 re sult of an overall stimulation of protein synthesis as other proteins are not affected. Exposure of the cells to antisense oligonucleotide t o jun, but not to sense oligonucleotide, reduces the increase in both jun and ChAT. These and previous results suggest that insulin is neces sary for the characteristic increase in ChAT protein during retina dev elopment and that this increase requires the transient synthesis of ju n. (C) 1997 Academic Press.