What an ancient jellyfish can teach us about the evoution of sleep

An upside-down jellyfish drifts in a shallow lagoon, rhythmically contracting its translucent bell. By night that beat drops from roughly 36 pulses a minute to nearer 30, and the animal slips into a state that, despite its lack of a brain, resembles sleep.

Field cameras show it even takes a brief siesta around noon, to “catch up” after a disturbed night.

A new Nature Communications study has tracked these lulls in cassiopea jellyfish, which belong to a 500 million year-old lineage, as well as in the starlet sea anemone nematostella. The study findings may help settle a long-running debate among biologists about what sleep is for.

Does sleep conserve energy, consolidate memories – or do something more biologically fundamental? Until recently, most evidence for a “house-keeping” role for sleep came only from vertebrates.

When mice sleep, brain and spinal cord fluid surges through the brain and washes away metabolic waste. And a 2016 mouse study found that some types of DNA breaks are mended more quickly during sleep. Time-lapse imaging in a 2019 study of zebrafish showed that sleep lets neurons (nerve cells) repair DNA breaks that build up during waking hours.

The new study showed for the first time that the same process occurs in some invertebrates. That while the jellyfish and sea anemone are awake, DNA damage accumulates in their nerve cells and when they doze, that damage is repaired.

The work pushes the origins of sleep back more than 600 million years, to before the cnidarian branch (jellyfish, anemones, corals) split from the line that led to worms, insects and vertebrates roughly 600–700 million years ago. It also gives weight to the idea that sleep began as a form of self-defence for cells.

The new work moves the discussion to creatures whose nervous systems are much simpler than ours and are little more than thin nets. If sleep repairs their neurons too, that function is probably fundamental because simpler nervous systems evolved first.

The researchers first had to figure out when a jellyfish or anemone is asleep. This is surprisingly tricky: even when they rest, bell muscles keep twitching or the polyp drifts in slow motion. To do this they filmed the animals under infrared light and flashed white light at them or a pulse of food (a tiny squirt of liquid brine-shrimp extract).

Jellyfish that had been pulsing below 37 beats per minute for at least three minutes, and anemones that had stayed still for eight minutes, reacted more slowly. This meets the “reduced responsiveness” criterion for sleep, which is the same across the animal kingdom.

Next, the scientists stained nerve cells in tissue taken from jellyfish in a lab tank to mark where DNA breakages happened. The number of breakages peaked at the end of each species’ active spell (mid-morning for the jellyfish and late afternoon for the anemone) and dropped after a long rest.

When the scientists kept the animals awake by changing the tank’s water currents, both the DNA breaks and the next day’s sleeping time increased, similar to classic “sleep rebound” in humans where your body catches up on sleep.

To test cause and effect, the team shone ultraviolet-B light, which damages DNA, on the animals. This treatment doubled the number of DNA breaks within an hour and prompted extra sleep later the same day. When the animals had dozed, the breaks reduced back toward baseline and the jellyfish resumed their usual daytime rhythm.

Melatonin, the overnight hormone familiar to jet-lag sufferers, was added to the tank water and caused both species to doze during what should have been their busiest stretch (daytime for the jellyfish, night-time for the anemone), leaving their usual rest period unchanged.

The new finding is surprising because melatonin’s soporific role was thought to have evolved alongside vertebrates with centralised brains and circadian rhythms that respond to light cues. Seeing it work in a brainless animal suggests that this evolution took place much longer ago.

Putting these pieces together, it seems wakefulness gradually stresses the DNA in nerve cells. Sleep offers a period of sensory deprivation during which repair enzymes that stitch or swap the components of DNA can work unimpeded.

This logic fits with experiments in fruit-flies and mice which have linked chronic sleeplessness to neurodegeneration. Insomnia has also been linked to build-ups of reactive oxygen molecules (highly reactive by-products of normal metabolism that can punch holes in DNA, proteins and cell membranes).

If jellyfish need sleep to keep their nerve nets intact, the need to sleep probably predates the evolution of brains, eyes and even bodies that are the same on both left and right sides. In evolutionary terms, a nightly repair window could have been vital. Ancient organisms that skipped it may have accumulated mutations in irreplaceable neurons and slowly lost control of movement, feeding and reproduction.

The new study tracked two species in the lab and one in a Florida lagoon, but cnidarians live in many different light levels and temperatures. To be able to generalise this finding, future work will need to confirm that DNA-repair during sleep happens in similar animals that live in different conditions such as cold, deep or turbid waters.

Does this study settle the debate? Not entirely. Sleep almost certainly carries more than one benefit. Tasks such as memory consolidation could have been layered onto an ancient physiological maintenance programme as nervous systems grew more complex.

Yet the new findings strengthen the view that guarding DNA is a core purpose of sleep.

Timothy Hearn does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.