High impact information on ric-8

• Exogenous application of phorbol esters or loss of DGK-1 (diacylglycerol kinase) rescues ric-8 mutant phenotypes [1].
• RIC-8 was genetically shown to act in concert with goa-1 to regulate centrosome movements in C. elegans . Interestingly, mammalian RIC-8 was recently found to behave as a GEF for Galpha subunits in vitro . We show that reduction of function of ric-8 results in a 1 cell embryo phenotype very similar to the phenotype of embryos depleted of Galpha [2].
• Further linking the two pathways, our epistasis analysis of a ric-8 null mutant suggests that RIC-8 (a receptor-independent G alpha guanine nucleotide exchange factor) is required to maintain both the G alpha(q) vesicle priming pathway and the neuronal G alpha(s) pathway in a functional state [3].
• Using transgene induction studies, we show that activating the G alpha(s) pathway in adult animals rapidly induces hyperactive locomotion and rapidly rescues the paralysis of the ric-8 mutant [4].
• 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 [5].

Biological context of ric-8

• 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 [5].

Anatomical context of ric-8

• 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 [5].

References