<p>The study provides the analysis of the physiological and histological alterations caused by heat stress in <i>Cladocora caespitosa</i>, an important bioconstructor species in the Mediterranean. The effects of heat stress on histology and molecular response (heat shock proteins and antioxidative markers) were compared in <i>C. caespitosa</i> from the natural environment (10°C) and after experimentally induced heat stress (20°C and 30°C) up to 2&#xa0;weeks. Histological comparison between corals in the natural environment and those exposed to 20°C reveals preservation of the cellular architecture, with mild changes in the surface layers, while corals exposed to 30°C displayed evident lesions in all tissue layers. Physiological changes observed <i>at</i> 20°C suggest that Hsp90 is utilised by <i>C. caespitosa</i> as the primary responsive heat shock protein, followed by Hsp60, with Hsp70 being the least responsive. Higher temperatures (30°C) caused elevated levels of reduced glutathione (GSH) antioxidative marker and downregulated Hsps, which can be linked with severe histopathological lesions and indicate repression of metabolic activity. Our results show that <i>C. caespitosa</i> has limited ability to adjust to quick thermal changes and prolonged heat waves and confirm ELISA method as appropriate and informative quantitate benchtop assay for biomonitoring research.</p>

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Effects of heat stress on Mediterranean endemic and endangered reef-building coral Cladocora caespitosa: study on physiological and histological markers

  • Pavel Ankon,
  • Vida Burić,
  • Domagoj Đikić,
  • Romana Gračan,
  • Irena Landeka Jurčević,
  • Silvestar Beljan,
  • Petar Kružić

摘要

The study provides the analysis of the physiological and histological alterations caused by heat stress in Cladocora caespitosa, an important bioconstructor species in the Mediterranean. The effects of heat stress on histology and molecular response (heat shock proteins and antioxidative markers) were compared in C. caespitosa from the natural environment (10°C) and after experimentally induced heat stress (20°C and 30°C) up to 2 weeks. Histological comparison between corals in the natural environment and those exposed to 20°C reveals preservation of the cellular architecture, with mild changes in the surface layers, while corals exposed to 30°C displayed evident lesions in all tissue layers. Physiological changes observed at 20°C suggest that Hsp90 is utilised by C. caespitosa as the primary responsive heat shock protein, followed by Hsp60, with Hsp70 being the least responsive. Higher temperatures (30°C) caused elevated levels of reduced glutathione (GSH) antioxidative marker and downregulated Hsps, which can be linked with severe histopathological lesions and indicate repression of metabolic activity. Our results show that C. caespitosa has limited ability to adjust to quick thermal changes and prolonged heat waves and confirm ELISA method as appropriate and informative quantitate benchtop assay for biomonitoring research.