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Vol. 9, Issue 6, 1367-1378, June 1998
*INSERM U385, Faculté de Médecine, 06107 Nice Cedex 2, France;
Up-regulation of the cAMP pathway by forskolin or Department of Pharmacology, Faculty of Medicine,
Kyoto University, Kyoto 606, Japan; and
§INSERM U452,
Faculté de Médecine, Nice, France
-melanocyte
stimulating hormone induces melanocyte and melanoma cell
differentiation characterized by stimulation of melanin synthesis and
dendrite development. Here we show that forskolin-induced dendricity is associated to a disassembly of actin stress fibers. Since Rho controls
actin organization, we studied the role of this guanosine triphosphate
(GTP)-binding protein in cAMP-induced dendrite formation. Clostridium botulinum C3 exotransferase, which inhibits
Rho, mimicked the effect of forskolin in promoting dendricity and
stress fiber disruption, while the Escherichia coli
toxin cytotoxic necrotizing factor-1 (CNF-1), which activates Rho and
the expression of a constitutively active Rho mutant, blocked
forskolin-induced dendrite outgrowth. In addition, overexpression of a
constitutively active form of the Rho target p160 Rho-kinase
(P160ROCK) prevented the dendritogenic effects of cAMP. Our
results suggest that inhibition of Rho and of its target
p160ROCK are required events for cAMP-induced dendrite
outgrowth in B16 cells. Furthermore, we present evidence that Rho is
involved in the regulation of melanogenesis. Indeed, Rho inactivation
enhanced the cAMP stimulation of tyrosinase gene transcription and
protein expression, while Rho constitutive activation impaired these
cAMP-induced effects. This reveals that, in addition to controlling
dendricity, Rho also participates in the regulation of melanin
synthesis by cAMP.
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