Harmful algal blooms in coastal marine and freshwater systems represent a serious and growing concern for human and wildlife health, particularly when these blooms of harmful algae that produce toxins. The invasive, bloom-forming alga Prymnesium parvum (aka, golden algae) has spread to more than 20 states in the last two decades, causing massive fish kills and threatening many inland recreational and commercial fisheries. While a good deal is known about the chemical nature and effects of golden algal toxins, less is understood with respect to why these toxins are produced, the mechanisms by which they are produced, or the means by which they are delivered to targeted organisms, such as fish. Researchers have long thought that golden algal toxins are produced during times of stress (as with a lack of sufficient nutrients) and released into the surrounding water to kill potential competitors and prey, thus freeing previously unavailable nutrients and alleviating the stress. In truth, however, this hypothesis is poorly supported by theoretical considerations and experimental data. This NSF-supported research challenges this long-standing paradigm of algal toxicity and, with the novel combination of experimentation with genetic, genomic, and analytical chemical approaches, aims to explicitly characterize how these toxins are produced and regulated, and how golden algae expose other organisms to these toxins. Expected results could transform the current toxicity paradigm and lead to significant future advances in the understanding of harmful algal blooms within the context of minimizing human and wildlife health risks associated with exposure to algal toxins.

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     Broadcast allelopathy, the prevailing paradigm in protistan toxicity, lacks convincing theoretical or experimental support. The objective of this NSF-supported research is to provide clear and meaningful analysis of toxin production and delivery in the toxigenic haptophyte Prymnesium parvum. The experimental approach is twofold, involving 1) novel analytical detection of toxins during predator-prey interactions, and 2) a genome-guided genetic foundation for toxigenesis and heterotrophic nutrient acquisition. The central hypothesis is that toxigenic protists use direct cell-to-cell contact for delivery of toxins and subsequent uptake and transport of prey cell constituents across the cell membrane. The underlying rationale of this research is the recent experimental demonstration that toxicity of P. parvum is mediated by direct prey contact, as well as the theoretical consideration that delivery of exotoxins by diffusion is unlikely, and not advantageous to the fitness of individual P. parvum cells. This research is significant because it will elucidate a fundamental process through which predation and heterotrophy are supported in toxigenic protists, and will thereby potentially transform the current toxicity paradigm by definitively identifying a mechanism for toxin delivery that would provide a fitness advantage without the need for group selection arguments. Results of this study will lead to future work focused on the mechanisms of protistan cell-cell interactions, physiological and biochemical action of protistan toxins, reassessment of the role of toxicity in bloom formation, and a model for exploring other toxigenic protistan taxa and the multitude of harmful algal toxins in aquatic systems.