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J Biol Chem, Vol. 273, Issue 44, 28700-28707, October 30, 1998
12, G13, and
Gq Induce Rho-dependent Neurite Retraction
through Different Signaling Pathways
,,,
From the Departments of In neuronal cells, activation of a certain
heterotrimeric G protein-coupled receptor causes neurite retraction and
cell rounding via the small GTPase Rho. However, the specific
heterotrimeric G proteins that mediate Rho-dependent
neurite retraction and cell rounding have not yet been identified. Here
we investigated the effects of expression of constitutively active G Molecular Neurobiology and
§ Physiological Chemistry, Faculty of Pharmaceutical
Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan
subunits on the morphology of differentiated PC12 cells. Expression of
GTPase-deficient G12, G13, and
Gq, but not Gi2, caused neurite
retraction and cell rounding in differentiated PC12 cells. These
morphological changes induced by G12,
G13, and Gq were completely inhibited by
C3 exoenzyme, which specifically ADP-ribosylates and inactivates Rho.
The tyrosine kinase inhibitor tyrphostin A25 blocked the neurite
retraction and cell rounding induced by G13 and
Gq. However, tyrphostin A25 failed to inhibit the
G12-induced neuronal morphological changes. On the other
hand, inhibition of protein kinase C or elimination of extracellular
Ca2+ blocked the neurite retraction and cell rounding
induced by Gq, whereas the morphological effects of
G12 and G13 did not require activation of
protein kinase C and extracellular Ca2+. These results
demonstrate that activation of G12, G13,
and Gq induces Rho-dependent morphological
changes in PC12 cells through different signaling pathways.
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