title: Changes in gene expression in gills of the euryhaline killifish Fundulus heteroclitus after abrupt salinity transfer.
abstract: Maintenance of ion balance requires that ionoregulatory epithelia modulate ion flux in response to internal or environmental osmotic challenges. We have explored the basis of this functional plasticity in the gills of the euryhaline killifish Fundulus heteroclitus. The expression patterns of several genes encoding ion transport proteins were quantified after transfer from near-isosmotic brackish water [10 parts/thousand (ppt)] to either freshwater (FW) or seawater (SW). Many changes in response to SW transfer were transient. Increased mRNA expression occurred 1 day after transfer for Na(+)-K(+)-ATPase-alpha(1a) (3-fold), Na(+)-K(+)-2Cl(-)-cotransporter 1 (NKCC1) (3-fold), and glucocorticoid receptor (1.3-fold) and was paralleled by elevated Na(+)-K(+)-ATPase activity (2-fold). The transient increase in NKCC1 mRNA expression was followed by a later 2-fold rise in NKCC protein abundance. In contrast to the other genes studied in the present work, mRNA expression of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel generally remained elevated (2-fold) in SW. No change in protein abundance was detected, however, suggesting posttranscriptional regulation. The responses to FW transfer were quite different from those to SW transfer. In particular, FW transfer increased Na(+)-K(+)-ATPase-alpha(1a) mRNA expression and Na(+)-K(+)-ATPase activity to a greater extent than did SW transfer but had no effect on V-type H(+)-ATPase expression, supporting the current suggestion that killifish gills transport Na(+) via Na(+)/H(+) exchange. These findings demonstrate unique patterns of ion transporter expression in killifish gills after salinity transfer and illustrate important mechanisms of functional plasticity in ion-transporting epithelia.
authors.affiliation: Department of Zoology, University of British Columbia, Vancouver, BC, Canada V6T 1Z4. scott@zoology.ubc.ca
authors.forename: Graham R
authors.initials: GR
authors.lastname: Scott
authors.forename: Jeff G
authors.initials: JG
authors.lastname: Richards
authors.forename: Biff
authors.initials: B
authors.lastname: Forbush
authors.forename: Paul
authors.initials: P
authors.lastname: Isenring
authors.forename: Patricia M
authors.initials: PM
authors.lastname: Schulte
mesh_terms: D000818:Animals; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics; D023781:Fundulidae / Q000502:physiology*; D015870:Gene Expression / Q000502:physiology; D005880:Gills / Q000502:physiology*; D006854:Hydrocortisone / Q000097:blood; D006180:Proton-Translocating ATPases / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D011965:Receptors, Glucocorticoid / Q000235:genetics; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride; D028021:Sodium-Potassium-Chloride Symporters / Q000235:genetics; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics; D064506:Solute Carrier Family 12, Member 2; D025262:Vacuolar Proton-Translocating ATPases / Q000235:genetics; D014882:Water-Electrolyte Balance / Q000502:physiology*
chemical_list: D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D028021:Sodium-Potassium-Chloride Symporters; D064506:Solute Carrier Family 12, Member 2; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D012965:Sodium Chloride; D012964:Sodium; D025262:Vacuolar Proton-Translocating ATPases; D006180:Proton-Translocating ATPases; D000254:Sodium-Potassium-Exchanging ATPase; D006854:Hydrocortisone