In Arctic-scale dramas played out under a microscope, the nematode worm Caenorhabditis elegans sometimes loses to a crafty hunter: the nematode-trapping fungus Arthrobotrys oligospora.
At first, it thrashes to escape the fungus’s lasso-like rings. Then, just as abruptly, the worm goes completely still – no crawling, no feeding, as if it has slipped into a deep sleep.
“We saw the worms initially struggling relentlessly for 15 to 20 minutes after being trapped, then suddenly stopping, as if they ‘gave up,” said Yen-Ping Hsueh, senior author of a recent study from Academia Sinica.
That striking switch set researchers at Academia Sinica (Taiwan) and the Max Planck Institute for Biology (Tübingen) on a hunt of their own: what in the worm’s nervous system flips that off switch?
Worms have a sleep survival switch
Few animals are as perfectly suited to this kind of sleuthing as C. elegans. It’s transparent, its 302 neurons are mapped like a subway, its genetics are exquisitely tractable, and its life cycle is fast.
Those advantages let the team probe predator-prey behavior at single-neuron resolution and pinpoint the circuitry behind the freeze.
The answer turned out to be a sleep circuit repurposed for survival. Physical capture makes the worm’s touch-sensing neurons light up. These signals relay the bad news to two sleep-promoting hubs in the brain – the ALA and RIS neurons.
Once engaged, those cells drive a quiescent, sleep-like state – motion and feeding shut down, energy use drops, and the worm waits.
“It’s a unique trigger of a sleep-like state caused by physically being caught by a predator,” explained first author Tzu-Hsiang Lin.
“The worm uses the same EGFR alarm system for other dangers, like being wounded or overheated. It’s activated by being physically caught.”
An ancient alarm system, redeployed
The “EGFR alarm system” Lin mentions is the epidermal growth factor receptor pathway, a stress-response signaling cascade conserved across animals. In C. elegans, EGFR links diverse stressors to the ALA/RIS sleep circuit.
Here, the team shows that tactile stress – being squeezed in a fungal noose – joins heat and injury to flip that switch.
Mechanosensation and EGFR work together as a two-key system. The worm has to sense the trap and send a distress signal before the shutdown begins.
That redundancy makes evolutionary sense. In a world without second chances, false alarms are costly. So is failing to power down when escape is impossible.
“Mechanosensation and EGFR signaling acting together reveal how animals carefully detect and respond to predators with complex behaviors,” Hsueh said.
The upshot is a picture of a highly versatile module: a sleep program that doubles as a last-ditch survival response.
Stillness as survival strategy
Why freeze at all? In mammals, freezing can lower detection by predators and buy time. For a worm glued in place, stillness might conserve energy, reduce further injury, or change the chemistry at the capture site. It might even interfere with the fungus’s next move.
The truth is, scientists don’t know yet whether quiescence helps the worm or the fungus. Lin is eager to find out.
“Who does freezing help? We need to figure out if this behavior actually helps the worm survive or if it just helps the fungus get its meal,” he said.
He and his colleagues also want to identify additional chemical signals that prime or sustain immobilization.
They also plan to test whether freezing is common across other nematodes and predatory fungi – clues to how widespread this strategy is in nature.
Genetics unlock predator-prey secrets
The idea that stress can induce sleep-like quiescence in worms has been around since the 1960s. But researchers didn’t yet have the tools to dissect both sides of this predator–prey interaction.
“The real opportunity came when both the worm and the fungus became easy to study with genetics, so we could finally dig into both sides of this predator-prey story,” Lin noted.
By combining precise neuronal manipulations in the worm with controlled encounters with Arthrobotrys, the team could separate cause from effect.
They showed that the touch input and EGFR pathway converge on ALA and RIS to produce the behavioral switch.
Worms reveal ancient predator strategy
This work reaches beyond nematodes and fungi. It underscores how evolution reuses core circuits – like sleep and stress pathways – for new purposes, including predator evasion.
It also adds detail to the growing view of sleep as an active, regulated state. Organisms can use it when needed, not just drift into it as a passive downtime.
“This opens a new window into how brains integrate external threats with internal states like sleep,” Hsueh said.
For neuroscientists, it’s a rare, cell-by-cell look at how a sensory cue becomes a decisive action. For ecologists, it’s a reminder that even simple animals carry sophisticated playbooks for survival.
And for the rest of us, it’s a bracing example of how much drama – and biology – lives at very small scales.
The study is published in the journal iScience.
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