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Toxicon. 2014 Feb;78:58-67. doi: 10.1016/j.toxicon.2013.11.011. Epub 2013 Dec 1.

Impact of elevated pCO₂ on paralytic shellfish poisoning toxin content and composition in Alexandrium tamarense.

Author information

1
Department of Aquatic Ecology, Netherlands Institute of Ecology (NIOO-KNAW), Post Office Box 50, 6700 AB Wageningen, The Netherlands; Marine Biogeosciences, Alfred Wegener Institute for Polar and Marine Research, Am Handelshafen 12, 27570 Bremerhaven, Germany. Electronic address: d.vandewaal@nioo.knaw.nl.
2
Marine Biogeosciences, Alfred Wegener Institute for Polar and Marine Research, Am Handelshafen 12, 27570 Bremerhaven, Germany. Electronic address: tim.eberlein@awi.de.
3
Ecological Chemistry, Alfred Wegener Institute for Polar and Marine Research, Am Handelshafen 12, 27570 Bremerhaven, Germany. Electronic address: uwe.john@awi.de.
4
Ecological Chemistry, Alfred Wegener Institute for Polar and Marine Research, Am Handelshafen 12, 27570 Bremerhaven, Germany. Electronic address: sylke.wohlrab@awi.de.
5
Marine Biogeosciences, Alfred Wegener Institute for Polar and Marine Research, Am Handelshafen 12, 27570 Bremerhaven, Germany. Electronic address: bjoern.rost@awi.de.

Abstract

Ocean acidification is considered a major threat to marine ecosystems and may particularly affect primary producers. Here we investigated the impact of elevated pCO₂ on paralytic shellfish poisoning toxin (PST) content and composition in two strains of Alexandrium tamarense, Alex5 and Alex2. Experiments were carried out as dilute batch to keep carbonate chemistry unaltered over time. We observed only minor changes with respect to growth and elemental composition in response to elevated pCO₂. For both strains, the cellular PST content, and in particular the associated cellular toxicity, was lower in the high CO₂ treatments. In addition, Alex5 showed a shift in its PST composition from a non-sulfated analogue towards less toxic sulfated analogues with increasing pCO₂. Transcriptomic analyses suggest that the ability of A. tamarense to maintain cellular homeostasis is predominantly regulated on the post-translational level rather than on the transcriptomic level. Furthermore, genes associated to secondary metabolite and amino acid metabolism in Alex5 were down-regulated in the high CO₂ treatment, which may explain the lower PST content. Elevated pCO₂ also induced up-regulation of a putative sulfotransferase sxtN homologue and a substantial down-regulation of several sulfatases. Such changes in sulfur metabolism may explain the shift in PST composition towards more sulfated analogues. All in all, our results indicate that elevated pCO₂ will have minor consequences for growth and elemental composition, but may potentially reduce the cellular toxicity of A. tamarense.

KEYWORDS:

Dinoflagellates; Gene regulation; Harmful Algal Blooms; Ocean acidification; Saxitoxin; Sulfur metabolism

PMID:
24291633
DOI:
10.1016/j.toxicon.2013.11.011
[Indexed for MEDLINE]
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