Implication of nitric oxide in the heat-stress-induced cell death of the symbiotic alga Symbiodinium microadriaticum

• Published in: Marine biology Vol. 156; no. 11; pp. 2209 - 2220
• Main Authors: Bouchard, Josée Nina, Yamasaki, Hideo
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer-Verlag 01.10.2009; Springer; Springer Nature B.V
• Subjects: Animal and plant ecology; Animal, plant and microbial ecology; Apoptosis; Biological and medical sciences; Biomedical and Life Sciences; Cell death; Cells; Climate change; Environmental conditions; Freshwater & Marine Ecology; Fundamental and applied biological sciences. Psychology; Global warming; Life Sciences; Marine & Freshwater Sciences; Marine biology; Marine organisms; Microalgae; Microbiology; Mortality; Nitric oxide; Oceanography; Original Paper; Phytoplankton; Plankton; Sea surface temperature; Sea water ecosystems; Synecology; Zoology; Programme Cell Death; Phytoplankton; Microalgae; Nitric Oxide; Dinoflagellate; Symbiosis; Temperature; Heat; Dinophyta; Cell death; Algae; Nitric oxide; Environmental factor; Stress
• ISSN: 0025-3162; 1432-1793
• DOI: 10.1007/s00227-009-1249-3

One of the major consequences of global warming is a rise in sea surface temperature which may affect the survival of marine organisms including phytoplankton. Here, we provide experimental evidence for heat-induced cell death in a symbiotic microalga. Shifting Symbiodinium microadriaticum from 27 to 32°C resulted in an increase in mortality, an increase in caspase 3-like activity, and an increase in nitric oxide (NO) production. The caspase-like activity was strongly correlated with the production of NO in thermally challenged microalgae. For this experiment, the application of Ac-DEVD-CHO, a mammalian caspase 3-specific inhibitor, partly prevented (by 65%) the increase in caspase-like activity. To verify the relationship between NO and the caspase-like activity, S. microadriaticum were subsequently incubated with 1.0 mM of the following chemical NO donors: sodium nitroprusside (SNP), S -nitrosoglutathione (GSNO), S -nitroso- N -acetylpenicillamine (SNAP) and 3,3bis(Aminoethyl)-1-hydroxy-2-oxo-1-triazene (NOC-18). The supplementation of both SNP and NOC-18 caused a significant increase in caspase-like activity compared to the control treatment. Pre-treatment of the microalgae with the inhibitor Ac-DEVD-CHO before the supplementation of the different NO donors completely prevented the increase in caspase-like activity. These results suggest that NO could play a role in the induction of cell death in heat-stressed S. microadriaticum by mediating an increase in caspase-like activity.