Mechanism: Under thermal and acidification stress, coral hosts increase ROS, selectively enriching rare microbiome taxa that scavenge ROS and promote calcification. Readout: Readout: This leads to preserved skeletal integrity and calcification rates, with rare taxa abundance increasing by 1500% under stress.
Hypothesis
Host cells under combined thermal and acidification stress increase production of reactive oxygen species (ROS) that selectively enrich rare microbiome taxa capable of degrading host-derived antioxidant compounds, thereby modulating the redox environment at the calcifying interface and preserving calcification rates.
Mechanistic basis
- Thermal stress triggers Symbiodiniaceae expulsion and ROS generation (see Oxidative Theory of Coral Bleaching) [https://pmc.ncbi.nlm.nih.gov/articles/PMC12835581/].
- Ocean acidification lowers pH, reducing carbonate ion availability and upregulating host proton pumps, which further elevates intracellular ROS via mitochondrial stress.
- Host ROS act as signaling molecules that upregulate expression of mucin-like glycoproteins and antimicrobial peptides, creating a niche favoring rare bacteria equipped with catalase, peroxidase, or alternative oxidase genes (e.g., rare Rhodobactereae and Microtrichales lineages).
- These rare taxa metabolize host-derived ROS and exude bicarbonate or organic carbon that can be transferred to the calcifying epithelium, locally raising pH and Ωaragonite.
- Consequently, corals with a microbiome enriched in ROS-scavenging rare taxa maintain higher calcification under combined stress, while those lacking this consortium show accelerated skeletal degradation.
Testable predictions
- Exposing Acropora fragments to elevated temperature (+2°C) and low pH (pH 7.8) will increase host ROS levels measured by DCFDA fluorescence within 48 h.
- 16S rRNA amplicon sequencing will reveal a significant rise in relative abundance of rare (<0.1% of community) bacterial OTUs possessing antioxidant genes (identified via metagenomic screening) compared to ambient controls.
- Inhibiting host ROS production with the antioxidant N-acetylcysteine will blunt the enrichment of these rare taxa and reduce calcification rates relative to untreated stressed fragments.
- Re-inoculating stressed fragments with a cultured consortium of ROS-degrading rare isolates will rescue calcification to near-control levels, whereas inoculating with a control bacterial mix will not.
Potential pitfalls
- Rare taxa may be below detection limits; using spike-in standards and long-read metagenomics can improve sensitivity.
- ROS measurements must be compartment-specific (surface mucus vs. tissue) to avoid confounding signals from symbiont photosynthesis.
- Scaling from fragment experiments to whole colonies requires accounting for flow-dependent nutrient exchange.
If falsified—i.e., no correlation between host ROS, rare taxon enrichment, and calcification preservation—then the hypothesis that host-driven oxidative priming selects for protective rare microbes would be rejected, prompting focus on alternative mechanisms such as direct ion-transport regulation or symbiont-mediated carbon recycling.
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