Implication of nitric oxide in the heat-stress-induced cell death of the symbiotic alga <Emphasis Type="Italic">Symbiodinium microadriaticum</Emphasis> |
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Authors: | Josée Nina Bouchard Hideo Yamasaki |
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Institution: | (1) Faculty of Science, University of the Ryukyus, Nishihara Okinawa, 903-0213, Japan;(2) Present address: National Oceanography Centre, University of Southampton, Waterfront Campus, European Way, Southampton, SO14 3ZH, UK |
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Abstract: | 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. |
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