Gill ionocyte remodeling mediates blood pH regulation in rockfish () exposed to environmentally relevant hypercapnia.

Marine fishes excrete excess H using basolateral Na-K-ATPase (NKA) and apical Na/H exchanger 3 (NHE3) in gill ionocytes. However, the mechanisms that regulate H excretion during exposure to environmentally relevant hypercapnia (ERH) remain poorly understood. Here, we explored transcriptomic, proteomic, and cellular responses in gills of juvenile splitnose rockfish () exposed to 3 days of ERH conditions (pH ∼7.5, ∼1,600 μatm Pco). Blood pH was fully regulated at ∼7.75 despite a lack of significant changes in gill ) mRNAs coding for proteins involved in blood acid-base regulation, ) total NKA and NHE3 protein abundance, and ) ionocyte density. However, ERH-exposed rockfish demonstrated increased NKA and NHE3 abundance on the ionocyte plasma membrane coupled with wider apical membranes and greater extension of apical microvilli. The observed gill ionocyte remodeling is consistent with enhanced H excretion that maintains blood pH homeostasis during exposure to ERH and does not necessitate changes at the expression or translation levels. These mechanisms of phenotypic plasticity may allow fishes to regulate blood pH during environmentally relevant acid-base challenges and thus have important implications for both understanding how organisms respond to climate change and for selecting appropriate metrics to evaluate its impact on marine ecosystems. Splitnose rockfish exposed to environmentally relevant hypercapnia utilize existing proteins (rather than generate additional machinery) to maintain homeostasis.