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Neuronal calcium sensor-1 (NCS-1) mediates changes in cellular function by regulating various target proteins. Many potential targets have been identified but the physiological significance of only a few has been established. Upon temperature elevation,  Caenorhabditis elegans  exhibits reversible paralysis. In the absence of NCS-1, worms show delayed onset and a shorter duration of paralysis. This phenotype can be rescued by re-expression of  ncs-1  in AIY neurons. Mutants with defects in four potential NCS-1 targets ( arf-1.1 ,  pifk-1 ,  trp-1  and  trp-2 ) showed qualitatively similar phenotypes to  ncs-1  null worms, although the effect of  pifk-1  mutation on time to paralysis was considerably delayed. Inhibition of  pifk-1  also resulted in a locomotion phenotype. Analysis of double mutants showed no additive effects between mutations in  ncs -1 and  trp-1  or  trp-2 . In contrast, double mutants of  arf-1.1  and  ncs-1  had an intermediate phenotype, consistent with NCS-1 and ARF-1.1 acting in the same pathway. Over-expression of  arf-1.1  in the AIY neurons was sufficient to rescue partially the phenotype of both the  arf-1.1  and the  ncs-1  null worms. These findings suggest that ARF-1.1 interacts with NCS-1 in AIY neurons and potentially  pifk-1  in the Ca 2+  signaling pathway that leads to inhibited locomotion at an elevated temperature.

Interaction of ARF-1.1 and neuronal calcium sensor-1 in the control of the temperature-dependency of locomotion in Caenorhabditis elegans