Analyses of molecular mechanisms of sensory processing in C.elegans

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Animals sense many environmental stimuli, and process these sensory information in the nervous system. This sensory processing includes processes for selection of appropriate information, proper integration, and modification by experience or memory. To elucidate molecular and neuronal mechanisms for sensory processing, we are studying mutants defective in sensory intimation and learning behavior.hen-1 mutants show defects in integration of two sensory signals Cu^<2+> and attractive odorants. hen-1 mutant animals slow weaker tendency to cross the Cu^<2+> barrier during migrating toward diacetyl, although they appear not to exhibit defects in chemotaxis to diacetyl nor avoidance of Cu^<2+>. Furthermore, hen-1 mutant animals show abnormality in behavioral plasticities induced by paired presentation of NaCl and starvation and of temperature and starvation. The hen-1 gene encodes a secretory protein with an LDLa motif which is most homologus to a Drosophila signaling molecule, Jeb. HEN-1 is expressed in ASE and AIY neurons and functions cell-non-autonomously in the mature nervous system.Recently, Jeb in Drosophila is reported to regulate development of mesodermal cells through a receptor tyrosine kinase, DAlk, which is a homologue of proto-oncogene, Alk. Since the LDLa domain in Jeb is similar to that in HEN-1, we started to analyze the scd-2 gene, which encodes a receptor tyrosine kinase similar to DAlk. scd-2 mutants show behavioral deflects same as hen-1 mutants in paradigms for sensory integration and learning.