Osmotic stress represents a limiting physical parameter for marine organisms and especially for sessile scleractinian corals which are known to be basically stenohaline and osmoconformers. The salinity changes may cause important cellular damage since corals lack any developed physiological regulatory system. One mechanism of reaction to deleterious conditions is the rapid increase of the induction of heat shock proteins. This study highlights the modulation of the expression of a mitochondrial heat shock protein, such as the chaperonin Hsp60, in the animal tissues of the scleractinian coral Seriatopora caliendrum under three salinity scenarios (hypersalinity of 45 ppt, hyposalinity of 25 ppt and extreme hyposalinity of 15 ppt). The study was performed during the time course of a 2-day period and accompanied also by the assessment of the coral health condition. For each salinity stress S. caliendrum responds differently at the morphological and cellular levels, since the Hsp60 exhibited specific patterns of expression and the coral showed different tissue appearance. Furthermore, the response reflects the severity and exposure length of the disturbance. However, the results indicate that S. caliendrum seems able to tolerates high salinity better than low salinity. In particular, in extreme hyposalinity conditions, a considerable gradual down-regulation of Hsp60 was detected accompanied by necrosis and degradation of the coral tissues. The study suggests that Hsp60 may be involved in the mechanisms of cellular response to stress caused by exposure to adverse salinity.
Keywords: Hsp60; Hypersalinity; Hyposalinity; Necrosis; Scleractinian corals; Seriatopora caliendrum; Stress.
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