FN Archimer Export Format
PT J
TI Inter-individual variability in freshwater tolerance is related to transcript level differences in gill and posterior kidney of European sea bass
BT 
AF L'Honoré, Thibault
   FARCY, Emilie
   Blondeau-Bidet, EVa
   Lorin-Nebel, Catherine
AS 1:1;2:1;3:1;4:1;
FF 1:;2:;3:;4:;
C1 Univ Montpellier, CNRS, IFREMER, IRD, UM, MARBEC, Montpellier, France
C2 UNIV MONTPELLIER, FRANCE
UM MARBEC
IN WOS Cotutelle UMR
IF 3.688
TC 12
UR https://archimer.ifremer.fr/doc/00614/72569/71524.pdf
LA English
DT Article
DE ;Intraspecific variation;Osmoregulation;Freshwater acclimation;Ion transporters;SLC26A6;NKCC;PRLR
AB 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. 
PY 2020
PD MAY
SO Gene
SN 0378-1119
PU Elsevier BV
VL 741
UT 000526116400015
DI 10.1016/j.gene.2020.144547
ID 72569
ER

EF