Ishii N et al. (1983) International C. elegans Meeting "effect of radiation on life-span of nematode."

Suzuki K, Ishii N

[International C. elegans Meeting, 1983]

Ishii N et al. (1985) International C. elegans Meeting "sensitivity of C elegans and R tokai embryos to X-rays."

Ishii N, Suzuki K

[International C. elegans Meeting, 1985]

Chun-Yi Huang et al. (2007) International Worm Meeting "eif-3.K is a pro-apoptotic gene in C. elegans."

Jia-Yun Chen, Yi-Chun Wu, Chun-Yi Huang

[International Worm Meeting, 2007]

Programmed cell death (or apoptosis) is an important feature of C. elegans development. Previous studies have identified pro-apoptotic genes egl-1, ced-3 and ced-4 and anti-apoptotic genes ced-9 and icd-1 that control programmed cell death.. We have identified and characterized a novel pro-apoptotic gene eif-3.K. Loss-of-function by mutation or RNAi inactivation in eif-3.K resulted in a decrease of cell corpses, whereas heatshock-induced over-expression of eif-3.K weakly but significantly increased cell corpses. Interestingly, the eif-3.K mutation partially suppressed ectopic cell deaths caused by over-expression of egl-1 or ced-4. This result suggests that eif-3.K may act downstream of or in parallel to egl-1 and ced-4 in the programmed cell death pathway. Using a cell-specific promoter to express eif-3.k in touch neurons, we showed that eif-3.K likely promoted cell death in a cell-autonomous manner. To further explore EIF-3.K function, we generated antibodies against bacterially expressed EIF-3.K protein. We found that EIF-3.K was ubiquitously expressed during embryogenesis and localized to the cytoplasm. As human eif-3.K can functionally substitute C. elegans eif-3.K in an eif-3.K mutant, the function of eif-3.K in apoptosis is likely conserved in evolution.

Hosokawa H et al. (1993) International C. elegans Meeting "Rapid accumulation of fluorescent material with aging in an oxygen-sensitive mutant mev-1 of Caenorhabditis elegans."

Hosokawa H, Suzuki K, Ishii N

[International C. elegans Meeting, 1993]

Suzuki N et al. (1993) International C. elegans Meeting "Cloning of manganese superoxide dismutase gene in C. elegans."

Suzuki N, Suzuki K, Ishii N

[International C. elegans Meeting, 1993]

Chun-Yi Huang et al. (2006) East Asia C. elegans Meeting "eif-3.K is a pro-apoptotic gene in C. elegans"

Teng-Wei Huang, Chun-Yi Huang

[East Asia C. elegans Meeting, 2006]

Programmed cell death or apoptosis is an important feature during C. elegans development. The pro-apoptotic genes egl-1, ced-4 and ced-3 are required for the execution of cell death. We have identified and characterized a novel pro-apoptotic gene eif-3.K. A loss-of-function mutation or inactivation by RNA interference in eif-3.K resulted in a reduction of cell corpse number during embryogenesis, whereas heatshock-induced over-expression of eif-3.K weakly but significantly promoted programmed cell death. In addition, eif-3.K mutation partially suppressed ectopic cell deaths caused by over-expression of egl-1 and ced-4. This result suggests that eif-3.K may act downstream of or in parallel to egl-1 and ced-4 in the genetic pathway during programmed cell death. Using a cell-specific promoter we showed that eif-3.K likely promoted cell death in a cell-autonomous manner. We generated antibodies against bacterially expressed EIF-3.K protein. The immunostaining result showed that EIF-3.K was ubiquitously expressed during embryogenesis and localized to the cytoplasm. To better understand the cell-death defect of eif-3.K mutants, we are currently performing a 4D microscopic analysis of the cell death process in wild-type and eif-3.K mutants.

Ishii N et al. (1991) International C. elegans Meeting "RAD-8 IS AN OXYGEN-HYPERSENSITIVE MUTANT."

Hartman PS, Suzuki N, Suzuki K, Ishii N

[International C. elegans Meeting, 1991]

Rad-8, isolated as a radiation (ultraviolet light)-sensitive mutants was also hypersensitive to methyl viologen and oxygen. The methyl viologen has been shown to reduce oxygen to superoxide anions and the superoxide anions produce hydrogen peroxide and hydroxyl radicals. Every one of these active oxygen species is toxic to living beings. The rad-8 mutant was about 8 times more sensitive to methyl viologen than the wild type comparing the concentrations causing 37% survival. Under 60% oxygen, almost 100% of wild-type animals suNived, while less than 1% of rad-8' mutants survived. The growth of rad-8 was about 2 times slower than the wild type and they produced a smaller number of zygotes even under atmospheric oxygen. The adults were also of smaller size than the wild-type adults. The time of zygote laying and the number of wild-type zygotes remained constant over the range of 5% to 50% oxygen, while the time of zygote laying and the number of the mutant zygotes varied with oxygen concentration. A wild-type animal started to produce zygotes on 3 days after hatching and had about 266 zygotes over the range of 5% to 40% oxygen, while mutants started to produce on 5 days after hatching and had 70 zygotes under atmospheric oxygen. Under low oxygen concentration (e.g., 5% oxygen) the time of zygote laying of the mutant was accelerated to 4 days and the number of zygotes was increased to 182, and under high oxygen concentration ( e.g., 50%) the time of zygotes laying was delayed to 7 days and the number of zygotes was reduced to 28.

Ishii N et al. (1993) International C. elegans Meeting "The effects of temperature on the longevity of a radiation-sensitive mutant, rad-8."

Suzuki N, Suzuki K, Ishii N, Hartman PS

[International C. elegans Meeting, 1993]

Yamasaki, Akira et al. (2017) International Worm Meeting "Effects of Region-Specific Irradiation on Locomotion and Autophagy in C. elegans."

Zhang-Akiyama, Qiu-Mei, Suzuki, Michiyo, Kobayashi, Yasuhiko, Yamasaki, Akira, Funayama, Tomoo

[International Worm Meeting, 2017]

Ionizing radiation generates reactive oxygen species, and causes damage to cell components including DNA and protein. In C.elegans, radiation sensitivity is different from germline-cell and somatic cell. When adult C.elegans are irradiated with ten-fold higher dose than the dose that leads to germline-cell death, worms are still alive1. Locomotion using motor neurons and body-wall muscles was reduced immediately after irradiation with 0.5 kGy2. However the mechanism of reduction is not fully understood. In the present study, to investigate a tissue that is responsible for reduction of locomotion, we used region-specific microbeam irradiation. We used energetic carbon ions delivered from the AVF cyclotron at Takasaki Ion accelerators for Advanced Radiation Application facility of QST-Takasaki. After irradiation, a worm was replaced on NGM plate, and the locomotion was video-recorded and then the trajectory for 5-sec duration was derived by image processing of the movie. As a result, the same effects as whole-body irradiation were not observed after region-specific microbeam irradiation to pharynx or anterior half-body (the nerve ring, pharynx, intestine, and gonad) or posterior or posterior half-body (vulva, intestine, gonad, and tail). This suggests that the radiation effects on locomotion depend on the size of irradiation area. To detect the dose whether the reduction of locomotion is restored or leads to individual death, and we investigated alternation of locomotion after irradiation. We found the dose that locomotion of worms were completely stopped immediately after irradiation, and had been stopped at least twenty-four hours. Less than the dose, locomotion of the worms was reduced in a dose dependent manner, and was partially restored after twenty-four hours. Protein damage generated by irradiation may be involved in this reduction and restoration of locomotion, so we investigated whether autophagy is induced after irradiation. Using GFP reporter assay of lgg-1, one of the autophagosome genes, the increased level of GFP::LGG-1 was detected seven hours after irradiation in somatic cells. This suggests that autophagy may be one of the reasons of restoration of locomotion after irradiation. 1. Ishii,N., Suzuki, K., Int. J. Radiat. Biol., 58:827-833. (1990) 2. Suzuki, M., et al., J. Radiat. Res. 50, 119-125. (2009)

Honda S et al. (1989) International C. elegans Meeting "an oxygen-sensitive mutant of C elegans and aging."

Ishii N, Honda S, Suzuki K, Matsuo M

[International C. elegans Meeting, 1989]