C. elegans</I> exhibits many types of behavioral plasticity, including associative learning behavior between cultivation temperature and feeding state (1). Well-fed animals cultivated with food migrate to their cultivation temperature on a temperature gradient, but starved animals cultivated without food avoid from their cultivation temperature. To elucidate the regulation mechanism of behavioral plasticity, we are using this temperature-food associative learning paradigm. The
aho-3(
nj15)</I> mutant has severe defect in this associative learning after cultivation at 23C; after cultivated at 23C at starved condition,
aho-3(
nj15)</I> mutants migrated to 23C and did not avoid 23C, while they showed normal response in food recognition. In addition,
aho-3(
nj15)</I> is defective in sensory integration of attractive and aversive stimuli, diacetyl and Cu2+, while they exhibit normal chemotaxis and avoidance to each of those stimuli. We found that
aho-3 </I>gene encodes a highly conserved protein among many species including human, although the molecular properties of which have not been characterized yet. AHO-3 has a predicted <font face=symbol>a</font>/<font face=symbol>b</font> hydrolase fold. The <font face=symbol>a</font>/<font face=symbol>b</font> hydrolase fold superfamily is one of the largest groups of enzymes with various catalyses, such as acetylcholinesterase, lipase, and serine carboxypeptidase (2, 3). The learning defect of
aho-3(
nj15)</I> was not rescued by expressing recombinant
aho-3</I> containing mutation into predicted catalytic residues, while the defect was rescued by expressing
aho-3</I>(wt). These results indicated that catalytic function of AHO-3 is important for the associative learning. GFP expression driven by
aho-3</I> promoter was observed in some sensory and interneurons, including AFD and AWC thermosensory neurons, AIY interneurons required for thermotaxis (4, 5), and ADF sensory neurons required for aversive learning (6). The defect of associative learning of
aho-3(
nj15)</I> was fully rescued by
aho-3</I> expression in ~40 pairs of sensory and interneurons, including AWC, and the defect was partially rescued by
aho-3</I> expression only in AWB and AWC. In order to elucidate the function of
aho-3</I> in the associative learning, we intend to identify an interactor of AHO-3 by using a yeast two-hybrid system, and to determine the alteration of neural activity in
aho-3(
nj15)</I> by using Ca2+ imaging. (1) Mohri et al.</I>, 2004, Genetics (2) Ollis et al.</I>, 1992, Protein Eng (3) Holmquist, 2000, Curr Protein Pept Sci (4) Mori and Ohshima, 1995, Nature (5) Kuhara et al.</I>, 2007, INWM (6) Zhang et al.</I>, 2005, Nature.