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J. Biol. Chem., Vol. 269, Issue 31, 19671-19674, Aug, 1994
M De Vivo and R Iyengar
We studied the effects of activation of the Gq-alpha signaling pathway on
mitogenesis by expressing a mutant (Q209L), activated alpha-subunit of Gq
(alpha q*) in NIH-3T3 cells. A clonal NIH-3T3 cell line expressing alpha q*
in an inducible manner was isolated. Expression of alpha q* is induced with
dexamethasone, allowing the use of non-induced cells as controls for the
effects of alpha q* expression. We found that, by itself, expression of
alpha q* did not increase either DNA synthesis or mitogen-activated protein
(MAP) kinase activity in serum- starved cells. Because alpha q* transforms
cells grown in the presence of serum (De Vivo M., Chen, J., Codina, J., and
Iyengar, R. (1992) J. Biol. Chem. 267, 18263-18266), we tested whether
growth factor- stimulated signaling and mitogenesis were affected by
expression of alpha q*. Platelet-derived growth factor (PDGF) stimulated
thymidine incorporation modestly (50%) in contact-inhibited, confluent cell
cultures. In cells expressing alpha q*, PDGF stimulated DNA synthesis up to
3-fold over basal. Concomitant with the potentiation of PDGF- stimulated
DNA synthesis, expression of alpha q* potentiated PDGF- stimulated p44 MAP
kinase activity. PDGF was much more effective in stimulating both DNA
synthesis and p44 MAP kinase activity in subconfluent cell cultures and
expression of alpha q* exerted little or no effect on PDGF-stimulated
effects in subconfluent cells. These data show that cooperation between
signaling pathways may occur in a cell state-specific fashion. Such
cooperation in part may be responsible for the triggering of complex
cellular responses such as cell transformation.
Activated Gq-alpha potentiates platelet-derived growth factor- stimulated mitogenesis in confluent cell cultures
Department of Pharmacology, Mount Sinai School of Medicine, City University of New York, New York 10029.
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