Thermosensation is essential for animal metabolism and behavior. We focus on thermotaxis to understand molecular mechanism underlying thermosensation. Loss-of-function (lf) mutation in
eat-16 encoding RGS, a negative regulator of G protein, causes cryophilic phenotype due to hyper activation of thermosensory signaling in AWC sensory neuron, which acts as thermosensory neuron besides its role as an olfactory neuron (1). As we previously reported, the cryophilic defect of
eat-16 mutant is suppressed by known mutations in G protein-coupled thermosensory signaling in AWC. To further identify new molecules involved in G protein-coupled thermosemsation, we isolated suppressors for cryophilic abnormality of
eat-16 by screening approximately 18000 genomes of
eat-16(N2), a
eat-16 strain with N2 background. In an attempt to map
nj69, one of the suppressor mutations, we used snip-SNPs with
eat-16(HA), a Hawaiian CB4856 strain containing
eat-16 mutation. We found that
nj69 mutation mapped between -12.67 and -8.61 on the chromosome X, based on the snip-SNPs result that that region was all N2 type DNA in strains which suppressed
eat-16 mutation. During the course of mapping, we found that
eat-16(HA) strain tends to show stronger cryophilic phenotype than that of
eat-16(N2) strain, implicating that this stronger cryophilicity may hide the suppression phenotype of
eat-16;
nj69 mutant. In mapping
nj69 mutation, strains showing stronger cryophilic phenotype have CB4856 type DNA at least between -11.77 and -10.52 on the chromosome X. Also, stronger cryophilic phenotype is dominant. To confirm whether stronger cryophilic phenotype was derived from unidentified factors in the CB4856 background on X chromosome, we made
eat-16 strains, in which the chromosome X is chimeric between N2 and CB4856 DNA types but other chromosomes are mostly N2. Additionally, to determine stronger cryophilic phenotype depends on
eat-16 or not, we are making strains carrying only chimeric X chromosome by removing
eat-16 mutation. (1) Kuhara, A., Okumura, M., et al., Science. 320:803 (2008).