Cystic fibrosis transmembrane conductance regulator in teleost fish

• Published in: BBA - Biomembranes 2002-11, Vol.1566 (1), p.16-27
• Main Authors: Marshall, W.S, Singer, T.D
• Format: Article
• Language: English
• Subjects: ABC cassette protein; Adaptation, Physiological; Amino acid similarity; Animals; Binding Sites; Brain; Brain - metabolism; Cloning, Molecular; Cyclic AMP - metabolism; Cyclic AMP-Dependent Protein Kinases - metabolism; Cystic Fibrosis Transmembrane Conductance Regulator - analysis; Cystic Fibrosis Transmembrane Conductance Regulator - genetics; Cystic Fibrosis Transmembrane Conductance Regulator - metabolism; Eel; Expression; Fishes - metabolism; Fugu; Fundulidae; Gene Expression Regulation; Gill epithelium; Gills - metabolism; Immunohistochemistry; Intestinal Mucosa - metabolism; Intestine; Ion channel; Killifish; Marine teleost; Phylogeny; Protein trafficking; Salmon; Seawater; Sequence Homology; Tilapia
• ISSN: 0005-2736; 0006-3002; 1879-2642
• DOI: 10.1016/S0005-2736(02)00584-9

The gills and intestinal epithelia of teleost fish express cystic fibrosis transmembrane conductance regulator (CFTR), and utilize this low conductance anion channel in the apical membrane for ion secretion in seawater gill and in the basolateral membrane for ion absorption in freshwater gill. Similarly, in the intestine CFTR is present in the basolateral membrane for intestinal absorption and also in the apical membrane of secreting intestine. The expression of CFTR and the directed trafficking of the protein to the apical or basolateral membrane is salinity-dependent. The CFTR gene has been cloned and sequenced from several teleost species and although all the major elements in the human gene are present, including two nucleotide binding domains that are common to all ATP binding cassette (ABC) transporters, the sequences are divergent compared to shark or human. In euryhaline fish adapting to seawater, CFTR, localized immunocytochemically, redistributes slowly from a basolateral location to the apical membrane while ion secretory capacity increases. The facility with which teleosts regulate CFTR expression and activation during salinity adaptation make this system an appealing model for the expression and trafficking operation of this labile gene product.