Abstract

Dinoflagellates are microscopic aquatic eukaryotes with huge genomes and an unusual cell regulation. For example, most genes are present in numerous copies and all copies seem to be obligatorily transcribed. The consequence of the gene copy number (CPN) for final protein synthesis is, however, not clear. One such gene is sxtA, the starting gene of paralytic shellfish toxin (PST) synthesis. PSTs are small neurotoxic compounds that can accumulate in the food chain and cause serious poisoning incidences when ingested. They are produced by dinoflagellates of the genera Alexandrium, Gymnodium, and Pyrodinium. Here we investigated if the genomic CPN of sxtA4 is related to PST content in Alexandrium minutum cells. SxtA4 is the 4th domain of the sxtA gene and its presence is essential for PST synthesis in dinoflagellates. We used PST and genome size measurements as well as quantitative PCR to analyze sxtA4 CPN and toxin content in 15 A. minutum strains. Our results show a strong positive correlation between the sxtA4 CPN and the total amount of PST produced in actively growing A. minutum cells. This correlation was independent of the toxin profile produced, as long as the strain contained the genomic domains sxtA1 and sxtA4.

Highlights

  • Genomic sxtA4 copy numbers in Alexandrium on it. Sommer et al (1937) demonstrated that the paralytic shellfish toxins (PSTs) were present in plankton samples containing A. catenella, that the PST content in the dinoflagellates varied and that it was likely to consist of more than one active substance

  • We focused on A. minutum, a globally distributed Alexandrium species that contains PST-producing and non-producing strains

  • Genome Size Measurements The A. minutum genome sizes are listed in Table 1 and ranged from 22.5 to 29.6 pg cell−1, with an average of 25.7 ± 1.9 pg cell−1 (n = 15)

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Summary

Introduction

Genomic sxtA4 copy numbers in Alexandrium on it. Sommer et al (1937) demonstrated that the paralytic shellfish toxins (PSTs) were present in plankton samples containing A. catenella, that the PST content in the dinoflagellates varied and that it was likely to consist of more than one active substance. Strains that do not produce any detectable amounts of PSTs have been reported to occur within otherwise PST-producing Alexandrium species Despite these advances, it is still not known how PST synthesis is regulated at a cellular level in dinoflagellates. The dinoflagellate Lingulodinium polyedra (Stein) Dodge has been reported to contain ∼30 copies of a protein kinase gene (Salois and Morse, 1997), 146 copies of the luciferase gene (Liu and Hastings, 2005), ∼1,000 copies of the Luciferin-binding Protein genes (Lee et al, 1993) and ∼5,000 copies of the mitotic cyclin gene (Bertomeu and Morse, 2004) The importance of these high gene CPNs for the cellular biology of dinoflagellates is not clear. It has been suggested that they may be related to the amount of protein that can be synthesized by a dinoflagellate cell (Lee et al, 1993, 2014; Moustafa et al, 2010)

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