A role for RIC-8 (Synembryn) and GOA-1 (G(o)alpha) in regulating a subset of centrosome movements during early embryogenesis in Caenorhabditis elegans.

RIC-8 (synembryn) and GOA-1 (G(o)alpha) are key components of a signaling network that regulates neurotransmitter secretion in Caenorhabditis elegans. Here we show that ric-8 and goa-1 reduction of function mutants exhibit partial embryonic lethality. Through Nomarski analysis we show that goa-1 and ric-8 mutant embryos exhibit defects in multiple events that involve centrosomes, including one-cell posterior centrosome rocking, P(1) centrosome flattening, mitotic spindle alignment, and nuclear migration. In ric-8 reduction of function backgrounds, the embryonic lethality, spindle misalignments and delayed nuclear migration are strongly enhanced by a 50% reduction in maternal goa-1 gene dosage. Several other microfilament- and microtubule-mediated events, as well as overall embryonic polarity, appear unperturbed in the mutants. In addition, our results suggest that RIC-8 and GOA-1 do not have roles in centrosome replication, in the diametric movements of daughter centrosomes along the nuclear membrane, or in the extension of microtubules from centrosomes. Through immunostaining we show that GOA-1 (G(o)alpha) localizes to cell cortices as well as near centrosomes. Our results demonstrate that two components of a neuronal signal transduction pathway also play a role in centrosome movements during early embryogenesis.