Host mTOR as a Civilization‑Survival Switch Governs Coral Holobiont Resilience via Autophagy‑Mediated Mucus Remodeling

Dr. Adam López (MD)· Mar 21, 2026

macro close-up of coral mucus membrane surface, intricate organic texture, translucent layers, soft diffuse lighting, microscopic bacterial ecosystem details

Hypothesis

Host mTOR activity acts as a civilization‑versus‑survival dial that determines whether the coral holobiont invests in skeletal growth and symbiont photosynthesis (civilization mode) or shifts to autophagy‑driven stress resistance and mucus remodeling (survival mode). Under combined thermal stress and ocean acidification, sustained mTOR activation inhibits the lysosomal transcription factor TFEB, blocking autophagy and reducing the secretion of mucin‑bound glycans that select for beneficial, ROS‑scavenging bacteria. Consequently, the mucus microbiome loses nitrogen‑cycling and vitamin‑producing taxa, while opportunistic pathogens proliferate, precipitating bleaching and mortality.

Mechanistic Rationale

mTORC1 phosphorylates and retains TFEB in the cytosol, preventing its nuclear translocation and the transcription of lysosomal and autophagy genes (https://academic.oup.com/jxb/article/73/20/6993/6609545).
In cnidarians, host mTOR integrates photosynthate from Symbiodiniaceae to drive calcification and anabolic metabolism (http://nbn-resolving.de/urn:nbn:de:bsz:352-2-168yqys8a9b3e7).
When mTOR remains active despite nutrient limitation or stress, the host continues to prioritize growth, depleting intracellular amino acid pools that would otherwise trigger AMPK‑ULK1‑mediated autophagy initiation.
Reduced autophagy diminishes autophagosome‑mediated secretion of mucin precursors and associated oligosaccharides, altering the chemical landscape of the coral surface mucus layer (https://researchportal.scu.edu.au/esploro/outputs/journalArticle/Rewiring-coral-Anthropogenic-nutrients-shift-diverse/991013138313702368).
Beneficial microbes that rely on host‑derived glycans for nitrogen acquisition and vitamin synthesis (e.g., Halomonadaceae, Rhodobacteraceae) lose their niche, while opportunistic vibrios that thrive on protein‑rich mucus dominate (https://academic.oup.com/femsre/article/47/2/fuad005/7071893).
The resulting dysbiotic mucus layer fails to scavenge ROS, amplifying oxidative damage to symbiont photosystems and accelerating bleaching.

Testable Predictions

Pharmacological inhibition of mTOR with rapamycin under heat‑acid stress will increase nuclear TFEB, elevate LC3‑II/autophagosome markers, and restore mucin‑glycan secretion compared with DMSO controls.
Genetic activation of host mTOR (e.g., constitutively active Rheb) will suppress TFEB nuclear localization, lower autophagy flux, and shift mucus metaproteome toward higher protein‑to‑carbohydrate ratios.
Microbiome sequencing of mucus from rapamycin‑treated corals will show enrichment of nitrogen‑fixing and vitamin‑B12 producing taxa, whereas mTOR‑hyperactive corals will exhibit increased relative abundance of Vibrio spp. and reduced diversity.
Bleaching outcomes (Fv/Fm decline, symbiont density loss) will be significantly attenuated in rapamycin‑treated fragments and exacerbated in mTOR‑hyperactive fragments after 7‑day exposure to 32 °C and pH 7.8.
Exogenous addition of purified host‑derived mucin glycans to mTOR‑hyperactive mucus will partially rescue the beneficial microbiome and ROS‑scavenging capacity, confirming that the glycan shift is a downstream effector of mTOR signaling.

Falsifiability

If rapamycin fails to increase TFEB nuclear localization or autophagy markers under stress, or if microbiome composition and bleaching severity do not diverge between mTOR‑modulated and control groups, the hypothesis that mTOR‑driven autophagy governs mucus‑mediated holobiont resilience would be refuted. Conversely, consistent support across these predictions would substantiate the civilization‑versus‑survival dial as a central control point for coral climate tolerance.

Hypothesis

Mechanistic Rationale

mTORC1 phosphorylates and retains TFEB in the cytosol, preventing its nuclear translocation and the transcription of lysosomal and autophagy genes (https://academic.oup.com/jxb/article/73/20/6993/6609545).

In cnidarians, host mTOR integrates photosynthate from Symbiodiniaceae to drive calcification and anabolic metabolism (http://nbn-resolving.de/urn:nbn:de:bsz:352-2-168yqys8a9b3e7).

When mTOR remains active despite nutrient limitation or stress, the host continues to prioritize growth, depleting intracellular amino acid pools that would otherwise trigger AMPK‑ULK1‑mediated autophagy initiation.

Reduced autophagy diminishes autophagosome‑mediated secretion of mucin precursors and associated oligosaccharides, altering the chemical landscape of the coral surface mucus layer (https://researchportal.scu.edu.au/esploro/outputs/journalArticle/Rewiring-coral-Anthropogenic-nutrients-shift-diverse/991013138313702368).

Beneficial microbes that rely on host‑derived glycans for nitrogen acquisition and vitamin synthesis (e.g., Halomonadaceae, Rhodobacteraceae) lose their niche, while opportunistic vibrios that thrive on protein‑rich mucus dominate (https://academic.oup.com/femsre/article/47/2/fuad005/7071893).

The resulting dysbiotic mucus layer fails to scavenge ROS, amplifying oxidative damage to symbiont photosystems and accelerating bleaching.

Testable Predictions

Pharmacological inhibition of mTOR with rapamycin under heat‑acid stress will increase nuclear TFEB, elevate LC3‑II/autophagosome markers, and restore mucin‑glycan secretion compared with DMSO controls.

Genetic activation of host mTOR (e.g., constitutively active Rheb) will suppress TFEB nuclear localization, lower autophagy flux, and shift mucus metaproteome toward higher protein‑to‑carbohydrate ratios.

Microbiome sequencing of mucus from rapamycin‑treated corals will show enrichment of nitrogen‑fixing and vitamin‑B12 producing taxa, whereas mTOR‑hyperactive corals will exhibit increased relative abundance of Vibrio spp. and reduced diversity.

Bleaching outcomes (Fv/Fm decline, symbiont density loss) will be significantly attenuated in rapamycin‑treated fragments and exacerbated in mTOR‑hyperactive fragments after 7‑day exposure to 32 °C and pH 7.8.

Exogenous addition of purified host‑derived mucin glycans to mTOR‑hyperactive mucus will partially rescue the beneficial microbiome and ROS‑scavenging capacity, confirming that the glycan shift is a downstream effector of mTOR signaling.

Falsifiability