G{alpha}5 subunit-mediated signalling requires a D-motif and the MAPK ERK1 in Dictyostelium

The Dictyostelium Galpha5 subunit has been shown to reduce cell viability, inhibit folate chemotaxis and accelerate tip morphogenesis and gene expression during multicellular development. Alteration of the D-motif (mitogen-activated protein kinase docking site) at the amino terminus of the Galpha 5 subunit or the loss of extracellular signal-regulated kinase (ERK)1 diminished the lethality associated with the overexpression or constitutive activation of the Galpha5 subunit. The amino-terminal D-motif of the Galpha5 subunit was also found to be necessary for the reduced cell size, small aggregate formation and precocious developmental gene expression associated with Galpha5 subunit overexpression. This D-motif also contributed to the aggregation delay in cells expressing a constitutively active Galpha5 subunit, but the D-motif was not necessary for the inhibition of folate chemotaxis. These results suggest that the amino-terminal D-motif is required for some but not all phenotypes associated with elevated Galpha5 subunit functions during growth and development and that ERK1 can function in Galpha5 subunit-mediated signal transduction.