COLOCALIZATION OF THE INSULIN-RECEPTOR, JUN PROTEIN AND CHOLINE-ACETYLTRANSFERASE IN EMBRYONIC CHICK RETINA

Previous work demonstrated that the availability of insulin to the emb ryonic chick retina at a critical developmental stage stimulated the a ctivity of the acetylcholine synthetic enzyme, choline acetyltransfera se (ChAT) and that this increase required the AP-1 transcription facto r, c-jun. Here it is shown that immediately following a 2-5 min exposu re to insulin there is, in the amacrine and ganglion cells of the chic k embryo retina, a transient increase in the level of jun protein foll owed by a long-lasting increase in ChAT. These and previous results sh ow that insulin receptor activation is necessary for the characteristi c retina developmental increase in ChAT protein and that this increase is preceded by a transient increase in the synthesis of the transcrip tion factor c-jun in the same retina cells. The data demonstrate an in tracellular signal transduction pathway from the developmentally-activ ated insulin receptor through c-jun to ChAT and cholinergic differenti ation. (C) 1998 Academic Press Limited.