V. Holdengreber et al., COLOCALIZATION OF THE INSULIN-RECEPTOR, JUN PROTEIN AND CHOLINE-ACETYLTRANSFERASE IN EMBRYONIC CHICK RETINA, Experimental Eye Research, 66(3), 1998, pp. 307-313
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.