Ocean acidification's impact on coral reefs is typically framed through the lens of reduced carbonate ion availability for calcification. However, the establishment of a reproducible in vitro coral-dinoflagellate symbiosis system (Pernice et al.) provides a tool to dissect earlier, cellular mechanisms of failure that precede skeletal dissolution. I propose that decreased external seawater pH directly remodels the lipid composition of coral host cell membranes, which in turn disrupts the proton balance within the symbiosome vacuole, leading to symbiont expulsion independent of thermal stress.

This hypothesis challenges the passive view of acidification as a mere "weakening" force. It posits an active, dysbiotic trigger rooted in cellular homeostasis. The rapid (5-minute) phagocytosis and high symbiosis rate in the Acropora tenuis model indicate a highly regulated intracellular environment. Maintaining a specific, slightly acidic pH (~5.5-6.0) in the symbiosome is critical for nutrient exchange and symbiont control. The coral cell must actively pump protons across the vacuolar membrane to maintain this gradient against the external environment. A sustained drop in external pH increases the proton motive force the cell must overcome.

The mechanistic link is membrane lipid remodeling. Under acidified conditions, cells across taxa often alter membrane fluidity and charge by incorporating more sterols or saturated fatty acids to reduce proton permeability. This is a speculative but testable extrapolation from general cellular stress biology. In coral host cells, such a global shift could inadvertently alter the function or localization of V-type ATPases—the primary proton pumps responsible for acidifying the symbiosome. If pump efficiency drops or membrane proton leak increases, the symbiosome pH would rise, becoming less acidic. A less acidic symbiosome impairs nutrient transfer (e.g., carbon movement from symbiont to host) and may compromise the host's ability to regulate symbiont division, triggering a dysbiotic cascade culminating in expulsion—a bleaching phenotype.

This model is falsifiable through targeted experiments using the in vitro system:

1. Direct Measurement: Culture coral cells in lowered pH seawater (e.g., pH 7.6) and directly measure symbiosome pH using pH-sensitive fluorescent dyes (e.g., LysoSensor). The prediction is a measurable alkalinization relative to controls (pH 8.1).
2. Lipidomics: Perform lipidomic profiling on coral cells exposed to acidification. The prediction is a significant shift toward more saturated phospholipids and increased sterol content.
3. Inhibitor Assays: Treat cells with specific inhibitors of membrane remodeling (e.g., inhibitors of fatty acid desaturases) under acidified conditions. If the hypothesis is correct, blocking this adaptation should accelerate symbiosis breakdown compared to untreated, acidified controls.

This shifts the paradigm: acidification may cause dysbiosis not by starving the skeleton first, but by corrupting the host cell's fundamental ability to maintain the intracellular niche that sustains its symbiotic partners. The bleaching event would be a consequence of failed cellular homeostasis, not just a secondary response to carbonate chemistry.