Salinity and prolactin regulate anoctamin 1 in the model teleost, Fundulus heteroclitus

To maintain internal ion balance in marine environments, teleost fishes leverage seawater (SW)-type ionocytes to actively secrete Na + and Cl - into the environment. It is well established that SW-type ionocytes utilize apically expressed cystic fibrosis transmembrane conductance regulator 1 (Cftr1) as a conduit for Cl - to exit the gill. Here, we investigated whether the Ca 2+ -activated Cl - channel, anoctamin 1 (Ano1), provides an additional path for Cl - -secretion in euryhaline mummichogs ( Fundulus heteroclitus). Two ano1 gene isoforms, denoted ano1.1a and -1.1b, exhibited higher expression in the gill and opercular epithelium of mummichogs long-term acclimated to SW versus fresh water (FW). Branchial ano1.1b and cftr1 expression was increased in mummichogs sampled 24 h after transfer from FW to SW; ano1.1a and -1.1b were upregulated in the gill and opercular epithelium following transfer from SW to hypersaline SW. Alternatively, the expression of ano1.1a, -1.1b, and cftr1 in the gill and opercular epithelium was markedly decreased after transfer from SW to FW. Given its role in attenuating ion secretion, we probed whether prolactin downregulates ano1-isoforms. In addition to attenuating cftr1 expression, a prolactin injection reduced branchial ano1.1a and -1.1b levels. Given how Ano1 mediates Cl - secretion by mammalian epithelial cells, the salinity- and prolactin-sensitive nature of ano1 expression reported here indicates that Ano1 may constitute a novel Cl - -secretion pathway in ionocytes. This study encourages a wider evaluation of this putative Cl - -secretion pathway and its regulation by hormones in teleost fishes.