Fig. 2.
Left-right AWC asymmetry is controlled by calcium. (A) Induction of left-right AWC asymmetry by lateral interactions. The AWCOFF default state is specified by calcium-MAPK signaling. Before cell-cell communication is initiated, AWC cells undergo a calcium influx through voltage-gated calcium channels. Calcium signaling activates the CaMKII-MAPK pathway, mediated by the TIR-1 adaptor protein, resulting in the inactivity of the str-2 promoter and in the AWCOFF state in both AWC cells. After axonal outgrowth, the NSY-5 innexin gap junction neuronal network and the NSY-4 claudin-like protein activate the Raw repeat protein OLRN-1 to antagonize the calcium-mediated signaling pathway in the AWC that will induce str-2 promoter activity and become AWCON. NSY-4 and NSY-5 are more active in the future AWCON cell than the future AWCOFF cell (see Fig. 3 and text for details). (B) Maintenance of left-right AWC asymmetry by transcriptional regulation. The NSY-7 transcription factor maintains str-2 promoter activity in the induced AWCON cell and represses AWCOFF genes, such as srsx-3 (not shown).