Intracellular acid-base regulation mediates a trade-off between shell and somatic growth in a clam under ocean...

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.