C. elegans can modify its thermotactic behavior in accordance with ambient conditions. After cultivation at a certain temperature with food, well-fed animals migrate to the cultivation temperature on a temperature gradient. By contrast, after cultivation without food, starved animals disperse and do not migrate to the cultivation temperature. We are using this thermotaxis behavior as an ideal paradigm to elucidate the mechanism of behavioral plasticity(1,2). We conducted genetic analysis with mutants that have abnormality in thermotaxis after starvation.
aho-3(
nj15),
odr-3(
n1605) and
gcy-28(
tm2411) mutants are defective in novel hydrolase, G protein alpha subunit and guanylyl cyclase, respectively(2,3,4,5). It was shown that
aho-3(
nj15),
odr-3(
n1605) and
gcy-28(
tm2411) mutants migrate to the higher temperature than their cultivation temperature after starvation(2,3,4).
ins-1(
nr2091) and
egl-4(
n479) mutants are defective in insulin-like peptide and cyclic GMP-dependent protein kinase, respectively, and both
ins-1(
nr2091) and
egl-4(
n479) mutants migrate to their cultivation temperature after starvation(6,7). To analyze genetic epistasis between these five mutations, we made double mutants.
aho-3 gcy-28,
aho-3;
odr-3 and
gcy-28;
odr-3 double mutants showed almost the same abnormality in the thermotactic behavioral plasticity as that of single mutants. Double mutants with
ins-1, namely,
aho-3;
ins-1,
odr-3;
ins-1 and
gcy-28;
ins-1 mutants showed intermediate abnormality when compared with two single mutants. These results imply that AHO-3, ODR-3 and GCY-28 can act in the similar pathway and that INS-1 can act in parallel with AHO-3, ODR-3 and GCY-28. Currently, we are trying to identify cellular or circuit site underlying starvation-induced thermotactic plasticity by conducting cell-specific rescue experiments.(1)Hedgecock and Russell, 1975, Proc. Natl. Acad. Sci. USA (2)Mohri et al., 2005, Genetics. (3)Nishio et al., 2009, International Worm Meeting. (4)Tsunozaki et al., 2008, Neuron. (5)Roayaie et al., 1998, Neuron. (6)Kodama et al., 2006, Genes Dev. (7)L'Etoile et al., 2002, Neuron.