Ocean Acidification

Highlights

• Clams actively regulate intracellular pH against ocean acidification via CAc
• RNAi confirms CAc’s essential role in H⁺ efflux, measured by in vivo SIET.
• A CAc-sAC-NKA network forms a conserved regulatory pathway for acid-base balance.
• DEB model shows this pH defense sustains shell linear growth despite metabolic costs.

SUMMARY

Ocean acidification (OA) is predicted to threaten marine bivalves, casting them as passive victims of changing carbonate chemistry. Contributing to a revised understanding, we identified a conserved mechanism for acid-base regulation that supports intracellular resilience. Using the Manila clam Ruditapes philippinarum as a model, this study demonstrated that intracellular pH (pH_i) homeostasis under elevated pCO₂ was maintained through cytosolic carbonic anhydrase (CAc)-mediated H⁺ efflux. A causal link was established by combining in vivo scanning ion-selective electrode technique (SIET) with RNA interference (RNAi), where RpCAc knockdown suppressed H⁺ efflux and compromised pH_i. A coordinated regulatory network involving CAc, soluble adenylyl cyclase (sAC), and Na⁺/K⁺-ATPase (NKA) was synergistically upregulated, suggesting an evolved adaptive pathway. Dynamic Energy Budget (DEB) modeling, calibrated with experimental data, revealed that this cellular compensation carries a high energetic cost, leading to a significant reallocation of resources: shell growth was maintained, but somatic growth was severely suppressed. These results elucidate a conserved cytoprotective mechanism that enables short-term tolerance of OA at a substantial somatic cost, redefining resilience to include energetic trade-offs.

Jiang W., Rastrick S. P., Xu D., Fang J., Li W., Yuan M., Du M., Gao Y., Strand Ø., Mao Y., Fang J. & Jiang Z., in press. Intracellular acid-base regulation mediates a trade-off between shell and somatic growth in a clam under ocean acidification. iScience. Article.