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The Journal of Neuroscience, October 1, 1999, 19(19):8498-8508

Essential Roles of c-JUN and c-JUN N-Terminal Kinase (JNK) in Neuregulin-Increased Expression of the Acetylcholine Receptor epsilon -Subunit

Jutong Si, Qi Wang, and Lin Mei

Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22908

Neuregulin is a neural factor implicated in upregulation of acetylcholine receptor (AChR) synthesis at the neuromuscular junction. Previous studies have demonstrated that the extracellular signal-regulated kinase (ERK) subgroup of MAP kinases is required for neuregulin-induced AChR gene expression. We report here that the neuregulin-mediated increase in AChR epsilon -subunit mRNA was a delayed response in C2C12 muscle cells. Neuregulin induced expression of immediate early genes c-jun and c-fos, which followed and depended on the ERK activation. Treatment of muscle cells with cycloheximide to inhibit c-JUN synthesis at the protein level and suppression of c-JUN function by a dominant-negative mutant blocked neuregulin-induced expression of the epsilon -subunit gene, indicating an essential role of c-JUN in neuregulin signaling. Furthermore, neuregulin activated c-JUN N-terminal kinase (JNK) in C2C12 muscle cells. Blockade of JNK activation by overexpressing dominant-negative MKK4 inhibited epsilon -promoter activation. Moreover, overexpression of the JNK dominant-negative mutant inhibited neuregulin-mediated expression of the epsilon transgene and endogenous epsilon -mRNA. Taken together, our results demonstrate important roles of c-JUN and JNK in neuregulin-mediated expression of the AChR epsilon -subunit gene and suggest that neuregulin activates multiple signaling cascades that converge to regulate AChR epsilon -subunit gene expression.

Key words: neuregulin; AChR; c-JUN; JNK; neuromuscular junction; synapse; immediate early gene

Copyright © 1999 Society for Neuroscience  0270-6474/99/19198498-11$05.00/0


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