DNA damage modulates sleep drive in basal cnidarians with divergent chronotypes

Jan 6, 2026Nature communications

DNA damage may change sleep need in simple animals with different daily activity patterns

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Abstract

Cassiopea andromeda and Nematostella vectensis sleep about one-third of the day, similar to humans.

Light and homeostasis primarily drove sleep in Cassiopea andromeda, which exhibited nocturnal sleep and midday naps.
Sleep in Nematostella vectensis was regulated by both the circadian clock and homeostatic processes, with increased sleep observed at dawn.
Melatonin promoted sleep in both species according to their specific sleep patterns.
Sleep deprivation, ultraviolet radiation, and mutagens were associated with increased neuronal DNA damage and sleep pressure.
Spontaneous and induced sleep appeared to support genome stability in both types of cnidarians.

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Sleep is a conserved behavior across all animals with a nervous system, ranging from cnidarians to humans. Considering the survival risks, why sleep evolved in basal lineages and what essential benefits it provides to the simple nerve net of nocturnal and diurnal invertebrates remain elusive. We used behavioral criteria to empirically define sleep in the upside-down jellyfish Cassiopea andromeda and the starlet sea anemone Nematostella vectensis. Light and homeostasis were the primary drivers of sleep in C. andromeda, which slept at night and napped at midday in both the laboratory and the natural habitat. In contrast, both the circadian clock and homeostatic processes regulated sleep in N. vectensis, which increased sleep at dawn. Similar to humans, C. andromeda, wild-type (WT) and Clock mutant (NvClk) N. vectensis slept about one-third of the day, irrespective of the daily timing and architecture of sleep, and melatonin promoted sleep in accordance with the species-specific chronotype. Notably, sleep deprivation, ultraviolet radiation, and mutagens increased neuronal DNA damage and sleep pressure, while spontaneous and induced sleep facilitated genome stability in both the diurnal and crepuscular cnidarians. These results suggest that DNA damage and cellular stress in simple nerve nets may have driven the evolution of sleep. Δ/Δ

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DNA damage modulates sleep drive in basal cnidarians with divergent chronotypes

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