Differential impacts of ocean acidification and alkalinization on shell microstructure and molecular responses in...

Anthropogenic CO₂ emissions are intensifying ocean acidification (OA), disrupting carbonate chemistry and threatening marine calcifiers such as mussels. Ocean alkalinity enhancement (OAE) has been proposed as a marine carbon dioxide removal (mCDR) strategy that can also mitigate OA, but its ecological safety for aquaculture species remains poorly understood. Here, we examined the short-term (21 days) responses of the blue mussel Mytilus edulis to OA (pH 7.3) and NaOH-based OAE (pH 9.0) using integrated shell microstructure analysis and transcriptomics. The results showed that while survival rates were unaffected, OA caused marked shell degradation and activated stress-related molecular pathways, whereas OAE enhanced shell integrity and stimulated growth-associated processes. Across treatments, a core set of biomineralization-related genes (e.g., VWA7, CA14, ALPL) exhibited expression shifts, suggesting central roles in carbonate homeostasis. In contrast, differential regulations of genes such as CA10 and VWDE revealed pH-specific responses. Notably, OAE induced minimal disruption of biomineralization and alleviated OA-related damage, highlighting its potential to support mussel aquaculture under future ocean conditions. While model simulations and plankton-scale experiments suggest global benefits of OAE, this study provides direct organism-level experimental evidence linking shell ultrastructure and transcriptomic responses under OA and OAE conditions. These findings offer mechanistic insights into mussel resilience and provide a critical empirical basis for evaluating the ecological safety of OAE as both a carbon sequestration strategy and a tool for sustainable aquaculture.