Evidence for disruption of Na super(+)-K super(+)-ATPase and hsp70 during vibriosis of sea bream, Sparus (=Rhabdosargus) sarba Forsskaal

• Published in: Journal of fish diseases 2005-04, Vol.28 (4), p.239-251
• Main Authors: Deane, E E, Woo, N Y S
• Format: Article
• Language: English
• Subjects: Marine
• ISSN: 0140-7775; 1365-2761
• DOI: 10.1111/j.1365-2761.2005.00624.x

Osmoregulation via the sodium pump (Na super(+)-K super(+)-ATPase) and cytoprotection via expression of different families of heat shock protein (hsp) were studied at transcriptional/translational levels during progressive vibriosis in silver sea bream, Sparus (=Rhabdosargus) sarba Measurements of Na super(+)-K super(+)-ATPase activity showed that an early and drastic decline occurred in the kidney of infected fish. This reduction in Na super(+)-K super(+)-ATPase activity was not caused by transcriptional downregulation of genes coding for either the Na super(+)-K super(+)-ATPase alpha or beta subunits. Using specific antibodies, data from immunoassays showed that the decreased sodium pump activity was caused by the specific loss of the translated glycosylated Na super(+)-K super(+)-ATPase beta subunit. Data from immunoassays of different hsp families demonstrated that the expression of hsp90 and hsp60 remained unchanged throughout vibriosis whereas expression of the hsp70 family decreased in kidney and liver tissues. As hsp70 is a multigene family, the expression of the constitutive (hsc70) and inducible (hsp70) members of the hsp70 family were studied and it was found that hsp70 and hsc70 expression decreased from an early stage of infection in the kidney and the liver respectively. Reverse transcriptase-polymerase chain reaction analysis of the hsp70 transcription-inducing factor, hsf1, demonstrated that loss of cytoprotective function during vibriosis was mediated by a downregulation of hsf1 transcription.