Hypothesis

Ocean acidification disrupts intracellular Ca²⁺ homeostasis in coral epithelium, which in turn modifies the activity of Golgi‑resident glycosyltransferases that decorate mucosal glycoproteins. The resulting shift toward sulfated, high‑mannose oligosaccharides creates a binding niche for opportunistic bacteria (e.g., Flavobacteriia, Chlamydiia) that precede the loss of Endozoicomonas and the onset of thermally induced dysbiosis. Thus, acidification‑driven mucus alteration is an early, measurable step that sensitizes the holobiont to subsequent heat stress.

Mechanistic Basis

1. Ca²⁺ signaling and glycosylation – Acidification lowers extracellular pH and perturbs Ca²⁺/H⁺ exchange (Corals in ocean acidification and the role of calcium ion…)[https://academic.oup.com/icesjms/article/82/4/fsaf050/8111516]. Elevated cytosolic Ca²⁺ activates Ca²⁺‑dependent protein kinases that phosphorylate glycosyltransferase regulators, biasing the glycan profile toward sulfated epitopes.
2. Mucus as a selective barrier – Coral mucus normally presents a glycan coat that favors mutualistic Endozoicomonas via specific lectin‑like interactions (Deciphering Coral Disease Dynamics: Integrating Host, Microbiome…)[https://www.frontiersin.org/journals/ecology-and-evolution/articles/10.3389/fevo.2020.575927/full]. Altered glycans reduce Endozoicomonas adhesion while increasing affinity for bacterial adhesins recognized by Flavobacteriia and Chlamydiia surface proteins.
3. Feed‑forward to dysbiosis – Early colonization by these taxa triggers local oxidative stress and mucinase activity, further degrading the mucus layer and facilitating symbiont expulsion when heat stress arrives (Defining Coral Bleaching as a Microbial Dysbiosis within the…)[https://pmc.ncbi.nlm.nih.gov/articles/PMC7692791/].

Testable Predictions

• Prediction 1: Corals exposed to reduced pH (∼7.6) for 2 weeks will show a significant increase in mucus‑bound sulfated glycans (detected by lectin blotting with SJIA and LEL) compared to controls at pH 8.1.
• Prediction 2: This glycan shift will correlate with a measurable rise in the relative abundance of Flavobacteriia and Chlamydiia in the mucus microbiome (16S rRNA amplicon sequencing) before any detectable loss of Endozoicomonas.
• Prediction 3: Subsequent thermal challenge (+2 °C above baseline) will induce bleaching earlier and more severely in acid‑treated fragments than in control fragments, and this difference will be abolished by enzymatic removal of sulfate groups from mucus (e.g., arylsulfatase treatment).
• Prediction 4: Inhibiting the Ca²⁺‑dependent kinase pathway (using a specific CaMKII antagonist) during acid exposure will prevent the glycan shift and the associated increase in opportunistic bacteria.

Experimental Approach

1. Fragment selection: Nubbins of Acropora hyacinthus and Porites lutea (species with known trophic plasticity) from a common garden.
2. Treatment groups: (a) ambient pH 8.1, (b) low pH 7.6, (c) low pH + CaMKII inhibitor, (d) low pH + aryl‑sulfatase post‑exposure.
3. Time‑series sampling: Days 0, 3, 7, 14 for mucus glycan analysis (HPLC‑MS of released oligosaccharides, lectin affinity), microbiome profiling (16S rRNA, qPCR for Endozoicomonas, Flavobacteriia, Chlamydiia), and Ca²⁺ imaging (Fluo‑4 AM).
4. Thermal stress: After 14 days, raise temperature to 30 °C for 48 h; quantify bleaching (chlorophyll fluorescence, photosynthetic efficiency) and symbiont density.
5. Statistical tests: Two‑way ANOVA (pH × inhibitor) for glycan scores; PERMANOVA for community shifts; regression linking glycan index to subsequent bleaching severity.

Implications

If confirmed, this hypothesis positions mucus glycosylation as a mechanistic bridge between ocean acidification and thermal bleaching, suggesting that interventions targeting mucosal glycan integrity (e.g., sulfide scavengers, glycosyltransferase modulators) could buy time for reefs under combined stressors. It also redirects focus from symbiont‑centric explanations to the host‑mediated biochemical environment that selects for pathogenic colonists prior to dysbiosis.