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

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.