Mechanism: Ocean acidification drives proton influx into coral cells, activating NHE and MAPK pathways, leading to thinner, less viscous mucus with reduced binding sites for beneficial Endozoicomonas bacteria. Readout: Readout: Mucus viscosity decreases, Endozoicomonas abundance drops by 80%, and opportunistic Proteobacteria increase, with alginate supplementation restoring mucus quality and beneficial bacteria.
Hypothesis Ocean acidification (OA) compromises the biophysical properties of coral mucus, reducing its capacity to host beneficial bacteria such as Endozoicomonas even when the coral harbors thermally tolerant symbionts like Durusdinium. This mucus‑mediated bottleneck lowers holobiont resilience to heat‑induced dysbiosis.
Mechanistic Rationale OA increases seawater pCO₂, driving proton influx across the coral epithelium. Elevated intracellular H⁺ activates Na⁺/H⁺ exchangers (NHE) to restore pH, which in turn alters cellular Ca²⁺ signaling and MAPK pathways that regulate mucin gene expression. The result is a thinner, less viscous mucus layer with altered polysaccharide composition and reduced antimicrobial peptide activity. These changes diminish binding sites for Endozoicomonas and favor opportunistic Proteobacteria.
Predictions
- Under low pH (≈7.6) and ambient temperature, corals will show decreased mucus thickness and viscosity compared to controls.
- The decline in mucus quality will correlate with lower Endozoicomonas relative abundance and higher ratios of opportunistic Proteobacteria, irrespective of symbiont type.
- When exposed to heat stress (e.g., +2 °C above ambient), corals under OA will experience faster onset of dysbiosis and higher disease incidence than those at ambient pH, even if they host Durusdinium.
- Supplementing mucus with exogenous polysaccharides (e.g., alginate) will rescue Endozoicomonas colonization and mitigate dysbiosis under OA + heat.
Experimental Design
- Factorial aquarium experiment with three factors: pH (ambient 8.1 vs low 7.6), temperature (ambient vs +2 °C), and symbiont type (Durusdinium vs Cladocopium).
- Use n = 6 replicate colonies per treatment (total 48).
- Measure after 4 weeks: mucus thickness (confocal microscopy), viscosity (rheometry), polysaccharide composition (HPAEC‑PAD), Endozoicomonas qPCR, Proteobacteria 16S amplicon sequencing, calcification rate (buoyant weight), and visual signs of disease/bleeding.
- In a sub‑set, add exogenous alginate to mucus surface to test rescue.
Potential Outcomes and Falsifiability
- If OA does not alter mucus properties or microbiome composition, the hypothesis is falsified.
- If mucus changes occur but do not affect Endozoicomonas abundance or disease outcomes, the mechanistic link is not supported.
- If alginate addition fails to rescue microbiome stability under OA + heat, the proposed binding‑site mechanism is questionable.
This framework directly tests the interaction highlighted in recent work—symbiont shifts Dynamic shifts in coral-Symbiodiniaceae partnerships, microbiome resilience Microbiome resilience in coral restoration—and addresses the noted gap on ocean acidification [OA underexplored](https://www.sciencedaily.com/releases/2025/07/250716000851.htm].
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