The mechanism by which polarity of the left-right (LR) axis is initially established with the correct handedness is not understood for any embryo. C. elegans embryos exhibit LR asymmetry with an invariant handedness that is first apparent at the six-cell stage and persists throughout development. We show here that a strong loss-of-function mutation in a gene originally designated spn-1 affects early spindle orientations and results in near randomization of handedness choice. This mutation interacts genetically with mutations in three par genes that encode localized cortical components. We show that the spn-1 gene encodes the Galpha protein GPA-16, which appears to be required for centrosomal association of a Gbeta protein. We will henceforth refer to this gene as gpa-16. These results demonstrate for the first time involvement of heterotrimeric G proteins in establishment of embryonic LR asymmetry and suggest how they might act.
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