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The role of carbonic anhydrase II on HCO3−‐initiated transport through the SLC4A4 transporter NBCe1A

The carbonic anhydrase II (CAII) metabolon hypothesis predicts that CAII binds to the electrogenic Na/HCO3 co‐transporter (NBCe1), enhancing its transport of HCO3−‐related species. In 2006, using a short I–V protocol (60 ms steps from the reversal potential Erev, 20 mV increments), the Boron Lab (BL) showed that neither pure CAII injected into Xenopus oocytes expressing NBCe1 nor CAII fused to the NBCe1 C‐terminus (Ct) changed NBCe1 slope conductance (G). Yet in 2007, using long I–V protocol steps and a holding potential (Vh) tens of mV from Erev, Becker & Deitmer (BD) concluded the opposite. We hypothesized that the CAII in the cytosol (rather than that attached to the membrane) enhanced transport in the BD protocol by dissipating long‐distance HCO3− and pHi gradients—an effect that should be accentuated by long Vh steps far from Erev. We found G was unchanged even after increasing Vh steps to 30 s, whether CAII was injected in the cytosol or fused to the NBCe1‐Ct. In fact, replicating the entire BD protocol detected no significant CAII‐mediated change in peak NBCe1 current (ΔI) or G. Even when NBCe1 was driven to near‐maximal activity by setting Vh at 0 mV, CAII did not enhance the recovery rate from CO2‐induced acidification, NBCe1 ΔI or G. These data contradict the metabolon hypothesis. We continue to test if the source of CAII protein or if NBCe1A expression levels can yield systematic differences in the effect of CAII on G.