Dauer larvae are non-aging developmental alternatives in the sense that post-dauer life spans are independent of the time spent as a dauer larvae (Klass, 1976). An interesting question is whether damage to molecular components during the dauer larval stage can influence post-dauer life span. In order to address this question, dauer larvae were exposed to X-radiation and life spans were subsequenctly determined. Interestingly, when young dauers (defined as animals that spent only a few days in this quiescent stage) were exposed to X-rays and incubated for some time before recovery, the post-dauer life spans were significantly prolonged. Even after receiving high doses (e.g., 500Gy), the life span tended to be longer than the control. On the other hand, when aged dauer larvae were irradiated and then allowed to immediately resume development, the level of longevity depended on the age of dauer larvae. The life span of the post-dauer larvae was not shorter than the control, even when 30-days-old dauer larvae were irradiated. When 20-day-old dauer larvae were irradiated, the levels of longevity depend on the time between irradiation and recovery. These differences may be due to subtle effects of storage conditions on post-dauer life span. The hormesis effect was lost in the dauer larvae when they were incubated for five days before recovery. This was an unexpected finding, but the repair system may be impoverished after extensive damage by X-ray irradiation at high doese. C. elegans dauer larvae may have an extremely high capacity of repair system with a hormesis effect relative to non-dauer larvae. The life extension effect was comparatively minimal even when L2 wild-type animals were irradiated at 100 Gy of X-ray. A subset of the genes such as
daf-2,
daf-16 and
age-1 are necessary for both dauer formation and determination of adult life span. These genes mediate the insulin-like signaling pathway. The strong repair system may be a key component of the longevity of these mutants. In contrast to wild-type animals, the life-extension effect was not presented even when L2
age-1 and
daf-16 mutants were irradiated at 100 Gy of X-ray. This suggests that the hormesis may be partly controlled by the insulin-like signaling pathway.