Calcium signaling and neuropeptide secretion in the expulsion step of the Caenorhabditis elegans defecation motor program
A periodic posterior to anterior intestinal calcium wave initiates the defecation motor program of Caenorhabditis elegans (C. elegans). innexin-16 (inx-16) encodes an intestinal pannexin gap junction subunit. inx-16 mutants have faulty calcium waves and mostly lack the expulsion step of the motor program. Our work investigates how these defective calcium waves result in loss of expulsion. The anterior-ventral neuron L (AVL) and dorsal-ventral neuron B (DVB) are responsible for expulsion through a two-step signaling process. An intestinal neuropeptide-like protein, NLP-40, activates AVL and DVB which in turn release neurotransmitters to stimulate expulsion. NLP-40 release likely depends on intestinal calcium flux, as vesicular localization of NLP-40 requires synaptotagmin-2. We propose that the expulsion defects in the inx-16 mutant are due to improper NLP-40 release. To establish if inx-16’s AVL and DVB neurons are functional, we used optogenetic methods. Activation of a light-gated ion channel channelrhodopsin-2 (ChR2) in AVL and DVB of inx-16 animals resulted in normal expulsion 90% of the time. This demonstrates that an inx-16 animal’s AVL and DVB neurons are able to signal expulsion and supports our hypothesis that defects in inx-16’s intestinal NLP-40 release inhibit expulsion. Current work addresses whether NLP-40 is properly synthesized and released.
McCright, Sam, and Maureen Peters. 2014. "Calcium signaling and neuropeptide secretion in the expulsion step of the Caenorhabditis elegans defecation motor program." FASEB Journal 28(1): 1129.6
Federation of American Society of Experimental Biology