Hypothesis

Ocean acidification lowers seawater pH, which increases the proportion of protonated dimethylsulfoniopropionate (DMSP) in the coral mucus layer. This acidic shift stimulates the expression of DMSP lyase genes in beneficial bacterial consortia (BMCs) such as Roseobacter and Phaeobacter spp., elevating the production of dimethyl sulfide (DMS) and acrylate. These volatile and semi‑volatile compounds act as infochemicals that diffuse into the coral tissue, where they are sensed by host G‑protein‑coupled receptor‑like proteins, triggering a signaling cascade that upregulates heat‑shock proteins (HSP70, HSP90), anti‑apoptotic Bcl‑2 family members, and innate immune effectors. Consequently, corals pre‑exposed to mild acidification exhibit a primed state that enhances thermal tolerance and reduces bleaching severity, an effect that is morphology‑dependent: massive corals already harbor higher baseline abundances of DMSP‑lyase‑positive bacteria, whereas branching corals lack this reservoir and thus benefit from exogenous BMC inoculation.

Mechanistic Reasoning

1. pH‑dependent substrate availability – At lower pH, the equilibrium DMSP ⇌ DMSP‑H⁺ favors the protonated form, which is a better substrate for the lyase enzyme (DddP/DddY) found in many marine alphaproteobacteria. Laboratory assays show a 2‑3‑fold increase in lyase activity when pH drops from 8.1 to 7.8 (analogous to future OA scenarios).
2. Bacterial signal amplification – Elevated DMSP lyase transcription raises intracellular DMS and acrylate concentrations. DMS can diffuse across bacterial membranes and, due to its low solubility, accumulates in the coral mucus–surface microlayer, reaching micromolar levels that are known to modulate eukaryotic signaling pathways.
3. Host reception – Coral genomes encode putative odorant‑binding receptors (OBRs) with homology to insect olfactory receptors that bind short‑chain sulfur compounds. Ligand binding activates phospholipase C, generating IP₃ and DAG, leading to calcium fluxes that activate MAPK cascades and downstream transcription factors (HSF1, NF‑κB) governing HSP and anti‑apoptotic gene expression.
4. Metabolic feedback – Increased host HSP70 stabilizes Symbiodiniaceae photosystem II, preserving Fv/Fm under heat stress, while reduced apoptosis limits symbiont loss. Concurrently, acrylate can be assimilated by the host as a carbon source, bolstering energy budgets during stress.
5. Morphological modulation – Massive corals exhibit thicker mucus layers and higher surface‑area‑to‑volume ratios, retaining more DMSP and facilitating prolonged bacterial exposure. Branching corals shed mucus more rapidly, diluting the signal and requiring higher bacterial densities to achieve equivalent host response.

Testable Predictions

• Prediction 1: In controlled aquaria, corals exposed to pH 7.8 for 7 days will show a significant increase (p<0.05) in bacterial dddP/dddY transcript levels (qPCR) relative to pH 8.1 controls, accompanied by a 1.5‑2× rise in dissolved DMS measured by gas chromatography‑mass spectrometry.
• Prediction 2: The rise in DMS will correlate with elevated host HSP70 and Bcl‑2 expression (RNA‑seq or Western blot) and reduced caspase‑3 activity under subsequent heat stress (32 °C for 48 h).
• Prediction 3: Blocking DMS synthesis with the lyase inhibitor allyl‑isothiocyanate will abolish the acidification‑induced increase in host stress‑protective genes, confirming the bacterial‑derived signal.
• Prediction 4: Massive species (e.g., Orbicella faveolata) will display a larger magnitude of HSP70 upregulation than branching species (e.g., Acropora cervicornis) under identical acidification‑pre‑treatment, and supplementation with a DMSP‑lyase‑enriched BMC cocktail will equalize the response across morphologies.
• Prediction 5: Field transplants of corals pre‑conditioned in low‑pH mesocosms will exhibit higher survival and lower bleaching scores after a natural heat wave compared with naïve controls, an effect that disappears when lyase‑knockdown bacteria are used for inoculation.

Falsification would occur if acidification fails to upregulate bacterial DMSP lyase, if DMS concentrations do not rise, or if host stress‑gene expression and survivorship remain unchanged despite these manipulations, indicating that the proposed DMS/acrylate signaling axis is not a primary mechanism linking ocean acidification to thermal tolerance.