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Background  The left and right AWC olfactory neurons in  Caenorhabditis elegans  differ in their functions and in their expression of chemosensory receptor genes; in each animal, one AWC randomly takes on one identity, designated AWC OFF , and the contralateral AWC becomes AWC ON . Signaling between AWC neurons induces left-right asymmetry through a gap junction network and a claudin-related protein, which inhibit a calcium-regulated MAP kinase pathway in the neuron that becomes AWC ON .    Results  We show here that the asymmetry gene  olrn-1  acts downstream of the gap junction and claudin genes to inhibit the calcium-MAP kinase pathway in AWC ON . OLRN-1, a protein with potential membrane-association domains, is related to the  Drosophila  Raw protein, a negative regulator of JNK mitogen-activated protein (MAP) kinase signaling.  olrn-1  opposes the action of two voltage-activated calcium channel homologs,  unc-2  (CaV2) and  egl-19  (CaV1), which act together to stimulate the calcium/calmodulin-dependent kinase CaMKII and the MAP kinase pathway. Calcium channel activity is essential in AWC OFF , and the two AWC neurons coordinate left-right asymmetry using signals from the calcium channels and signals from  olrn-1 .    Conclusion   olrn-1  and voltage-activated calcium channels are mediators and targets of AWC signaling that act at the transition between a multicellular signaling network and cell-autonomous execution of the decision. We suggest that the asymmetry decision in AWC results from the intercellular coupling of voltage-regulated channels, whose cross-regulation generates distinct calcium signals in the left and right AWC neurons. The interpretation of these signals by the kinase cascade initiates the sustained difference between the two cells.

neural development

Left-right olfactory asymmetry results from antagonistic functions of voltage-activated calcium channels and the Raw repeat protein OLRN-1 in C. elegans