Snodprot, which was a member of the cerato-platanin family, was found to change the chemotaxis and increase the body-bend frequency of Caenorhabditis elegans in a concentration-dependent manner in the study on the identification of snodprot gene of nematophagous fungi Dactylellina cionopaga (Yu et al., 2012). In L1 growth assay, stain with SYBR Green and lethality assay, snodprot did not affect the growth of the nematodes and kill the cells or the nematodes. The protein presented to reverse the functions of serotonin, but could not reverse the functions of octopamine, an antagonist of serotonin.

The chemotaxis-changing mechanism of snodprot might involve related neurons, the downstream signal transduction pathway, and regulatory elements because the attraction substance applied in this chemotaxis assay was NaCl. In the water-soluble chemotaxis of C. elegans ASE was the major neuron, and there was a weak residual response distributed over numerous classes of neurons, including ADF, ASG, ASI, ASK, and ASJ ( Bargmann, 2006). The signal transduction of ASE involved tax-4, tax-2, daf-11, and cGMP, the regulators of which are osm-9, gpc-1, tax-6, ttx-4, and adp-1. The receptors and the corresponding G proteins of the salts and water-soluble attractants might have been guanylate cyclases and gpa-3 (Bargmann, 2006).

The neurotransmitter serotonin regulates a wide range of behaviors in C. elegans, including egg laying, male mating, and locomotion (inhibition of movement) besides pharyngeal pumping (Chase and Koelle, 2007). The fact that snodprot could increase the locomotion of the nematodes significantly and in a concentration-dependent manner is consistent with the results of reversing the functions of serotonin of the protein. Expression of F01E11.5 (tyra-2), the receptor for serotonin and octopamine, was identified in pharyngeal neurons MC and NSM, amphid neurons ASE, ASG, ASH, ASI, and other neurons, including PVD, CAN, and ALM (Chase and Koelle, 2007).

The neurons are highly interconnected, and the neural networks for the exploratory and taxis behaviors partially overlap (White et al., 1986; Samuel and Sengupta, 2005). The transition to travelling search can involve the ASI, ASE, ADF, and ASH sensory neurons. The prominent targets of the ASE and AIY interneurons and additional targets, including the AIA and AIB interneurons of C. elegans, all regulate pirouettes (Bargmann, 2006). Samuel and Sengupta have also reported that the major neuronal components of the sensorimotor circuits of C. elegans, which mediate local search and long-range roaming behaviors, include chemosensory neurons ASI, AWC, and ASK, and interneurons AIB and AIY (Samuel and Sengupta, 2005).

It can be concluded that both ASE and ASI neutrons are involved in the process of chemotaxis to NaCl, the response to serotonin, and the locomotion of C. elegans. Thus the mechanism affected by snodprot is to be expected to combine competitively with serotonin in ASE or ASI neurons though the definitive combination site of snodprot awaits the confirmations of the immunity precipitation and other experiments.