Sassa, Yutaro et al. (2009) International Worm Meeting "A role of PKC-1 in regulation of aging in C.elegans."

Ohara, Yoshiyasu, Itakura, Satoshi, Kume, Kazunori, Mizunuma, Masaki, Sassa, Yutaro, Hirata, Dai, Miyahara, Kohji

[International Worm Meeting, 2009]

We have found that GEI-1-RHO-1 signal-transduction pathway regulates the olfactory adaptation in AWC sensory neuron, and that PKC-1, which has been shown to affect chemotaxis and thermotaxis, acts in the downstream of the GEI-1-RHO-1 pathway. On the other hand, it has been shown that insulin-like signaling pathway plays an important role for not only adaptation in the ASER salt-sensing neuron but also regulation of aging. Therefore, we focused on the functional relationship between olfactory adaptation and aging. To investigate whether or not the gene(s) concerned with the olfactory adaptation, which performs in sensory neurons, plays an important role in regulation of aging, we measured the life-span of the mutants related to GEI-1-RHO-1 signaling pathway. We found that the life-span in pkc-1 mutant is extended compared with wild-type strain. This extended life-span was dependent on DAF-16/FOXO. Consistent with the life-span, pkc-1 mutant was resistant to oxidative stress. Further, the expression of pkc-1wt in AWC neuron in pkc-1 mutant rescued the chemotaxis defects but not the extended life-span. These results suggest that PKC-1 plays an important role on regulation of aging, and that the regulation requires the expression of PKC-1 in the other cells except AWC neuron, or in both AWC and the others.

Ohara, Yoshiyasu et al. (2009) International Worm Meeting "Role of Rho GTPase signaling in olfactory adaptation."

Hirata, Dai, Kobuna, Hiroyuki, Motoshige, Kotaro, Kume, Kazunori, Ohara, Yoshiyasu, Gosho, Masayuki, Miyahara, Kohji, Tanaka, Sadaaki, Itakura, Satoshi, Sassa, Yutaro, Arai, Hiroyuki, Inoue, Takao

[International Worm Meeting, 2009]

We are interested in olfactory adaptation, a component of behavioral plasticity. To investigate the gene(s) involved in olfactory adaptation, we screened for the mutants defective in adaptation to odorants. From out of 4,000 EMS-mutagenized animals, we isolated 11 mutants exhibiting defects in adaptation to the AWC-sensed odorants. One of the mutants turned out to contain a mutation in gei-1, that encodes Rho-GAP (GTPase-activated protein). To investigate whether Rho-GTPase(s) acts in this behavior, we examined olfactory adaptation of transgenic animals expressing dominant active/negative forms of Rho-GTPase family. The dominant active RHO-1 inhibited normal olfactory adaptation as the gei-1 mutant. Furthermore, the genetic analyses indicate that RHO-1 acts downstream of GEI-1 and UNC-13 acts downstream of RHO-1 in olfactory adaptation. Next, to investigate whether the neurotransmitter Acetylcholine is important for the olfactory adaptation, we examined the effect of levamisole (activating Acetylcholine receptor) on the olfactory adaptation of wild-type strain. We found that the levamisole-treatment perturbs normal olfactory adaptation.