C.elegans locomotes backward when given the single tap stimulation. When given these stimuli repetitively the response gradually attenuates and the animals fall into the habituated state. To evaluate the mechanisms involved in habituation behavior, we isolated a mutant,
hab-1 (
cn308) showing abnormal in both acquirement and retention of habituation. We mapped the gene by two- and three-factor crosses with morphological and SNP markers(1). By rescue experiments, we found Y63D3A.7 was able to rescue the
hab-1 mutant phenotype. The fragment includes an open reading frame containing the mammalian B8 subunit homologue of mitochondrial complex I. The
hab-1 mutant shows increased resistance to rotenone, a potent NADH:ubiquinone oxidoreductase inhibitor. The
hab-1(
cn308) has a missense mutation at a highly conserved Glu residue to Gly. This
hab-1 mutant is sensitive to volatile anesthetics, showing a similar pattern as that of the
gas-1 mutant. The
hab-1 mutant is resistant to AChE inhibitors such as aldicarb or trichlorfon, indicating that the
hab-1 mutant is decreased in neurotransmitter release. To test if the
hab-1 mutant is defective in synaptic transmission, we are quantifying whole-cell voltage clamp currents recorded from the sensory neuron-interneuron junction of dissected nematodes. The
hab-1 gene expression might be developmentally regulated. Because the content of 15 kDa HAB-1 is increased in accompanying with the progress of development. Interestingly, the
cn308 HAB-1 is present more abundantly than the wild-type product. The mutant HAB-1 may be stable, though the enzyme activity is partially decreased. (1) X. Xu., et al., J. Neurogenetics 16: 1-16, 2002