Inter-individual variability in freshwater tolerance is related to transcript level differences in gill and posterior kidney of European sea bass

Type Article
Date 2020-05
Language English
Author(s) L'Honoré Thibault1, Farcy Emilie1, Blondeau-Bidet Eva1, Lorin-Nebel Catherine1
Affiliation(s) 1 : Univ Montpellier, CNRS, IFREMER, IRD, UM, MARBEC, Montpellier, France
Source Gene (0378-1119) (Elsevier BV), 2020-05 , Vol. 741 , P. 144547 (11p.)
DOI 10.1016/j.gene.2020.144547
WOS© Times Cited 4
Keyword(s) Intraspecific variation, Osmoregulation, Freshwater acclimation, Ion transporters, SLC26A6, NKCC, PRLR
Abstract

Acclimation to low salinities is a vital physiological challenge for euryhaline fish as the European sea bass Dicentrarchus labrax. This species undertakes seasonal migrations towards lagoons and estuaries where a wide range of salinity variations occur along the year. We have previously reported intraspecific differences in freshwater tolerance, with an average 30% mortality rate. In this study, we bring new evidence of mechanisms underlying freshwater tolerance in sea bass at gill and kidney levels. In fresh water (FW), intraspecific differences in mRNA expression levels of several ion transporters and prolactin receptors were measured. We showed that the branchial Cl-/HCO3- anion transporter (slc26a6c) was over-expressed in freshwater intolerant fish, probably as a compensatory response to low blood chloride levels and potential metabolic alkalosis. Moreover, prolactin receptor a (prlra) and Na+/Cl- cotransporter (ncc1) but not ncc-2a expression seemed to be slightly increased and highly variable between individuals in freshwater intolerant fish. In the posterior kidney, freshwater intolerant fish exhibited differential expression levels of slc26 anion transporters and Na+/K+/2Cl- cotransporter 1b (nkcc1b). Lower expression levels of prolactin receptors (prlra, prlrb) were measured in posterior kidney which probably contributes to the failure in ion reuptake at the kidney level. Freshwater intolerance seems to be a consequence of renal failure of ion reabsorption, which is not sufficiently compensated at the branchial level.

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