We hypothesize that mTORC1 activity in symbiont‑bearing host cells oscillates on a roughly 24‑hour rhythm, and that these pulses synchronize host cell proliferation with symbiont division to optimize photosynthate exchange and maintain holobiont homeostasis. In the civilizational state (high mTOR), host cells drive anabolic processes—ribosome biogenesis, lipid synthesis, and extracellular vesicle (EV) release—that expand the symbiosome membrane and provision nutrients to zooxanthellae. In the survival state (low mTOR), autophagy is activated to recycle damaged proteins and lipids, limiting oxidative stress and preventing EV overload. The alternation creates a metabolic window where growth phases build symbiotic capacity while clearance phases remove stress‑induced damage, a balance that chronic mTOR suppression or activation disrupts.

This dynamic coupling extends the civilization‑versus‑survival dial concept by adding a temporal dimension: the holobiont does not simply switch between modes but cycles through them, much like a cellular circadian clock. We propose that the mTOR pulse is entrained by the light‑dark cycle and reinforced by redox‑sensitive AMPK signaling, which rises during the night phase to transiently inhibit mTORC1 and trigger autophagic flux. When this rhythm is intact, susceptible species such as Orbicella faveolata can still mount a protective autophagy burst during infection, whereas disease‑tolerant Porites spp. exhibit higher amplitude oscillations that allow rapid return to growth after stress.

Testable predictions

1. Oscillation detection – A fluorescent mTORC1 activity reporter (e.g., mTORC1‑KTR) expressed in Aiptasia or coral larvae will show reproducible ~24‑hour peaks and troughs under normal light‑dark cycles (12 h : 12 h, 26 °C).
2. Stress disrupts rhythm – Exposure to thermal stress (30 °C) or acidified seawater (pH 7.7) will dampen oscillation amplitude and shift the phase toward a constitutively low‑mTOR state in bleaching‑susceptible species, while tolerant species maintain rhythmicity.
3. Pulsatile pharmacotherapy rescues symbiosis – Applying rapamycin in 1‑hour pulses every 12 hours (mimicking the natural trough) to stressed organisms will restore mTOR oscillation amplitude, increase autophagic flux (measured by LC3‑II/I ratio), elevate EV release (tracked by CD63‑GFP vesicles), and improve symbiont density, photosynthetic efficiency (Fv/Fm), and calcification rates compared with continuous rapamycin or vehicle controls.
4. Loss of oscillation predicts dysbiosis – Artificially flattening mTOR activity using a constitutively active Rheb construct will abolish oscillations, lead to either uncontrolled growth (high EV shedding, symbiont overproliferation) or excessive autophagy (symbiont loss), and result in disrupted microbiome composition (increase in pathogenic prokaryotes) as shown by 16S rRNA sequencing.

Mechanistic insight – We further speculate that mTOR‑driven EV release carries host‑derived pattern‑recognition receptors and lipid cargo that modulate symbiont immune evasion and membrane expansion during the growth phase. Conversely, the autophagy‑dominant low‑mTOR phase degrades excess EVs and damaged organelles, preventing vesicle accumulation that could trigger inflammasome activation. This EV‑autophagy coupling provides a concrete link between metabolic state and microbiome stability, explaining why both chronic mTOR inhibition (insufficient EV supply) and chronic activation (EV overload) produce dysbiosis.

Falsification – If high‑resolution live imaging reveals no detectable mTORC1 rhythm in symbiont‑bearing cells, or if restoring pulsatile mTOR activity fails to improve symbiont retention, ROS handling, or survival under stress, the hypothesis would be refuted. Conversely, confirmation would support a model in which longevity interventions must preserve, rather than abolish, the natural mTOR pulsatility that underpins the civilization‑survival trade‑off in complex holobionts.