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A spontaneous mutant of microcystin biosynthesis: genetic characterization and effect on Daphnia

Authors

  • Melanie Kaebernick,

    1. School of Microbiology and Immunology, University of New South Wales, Sydney 2052, Australia.
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  • Thomas Rohrlack,

    1. Freshwater Biological Laboratory, University of Copenhagen, Helsingørsgade 51, DK-3400 Hillerød, Denmark.
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  • Kirsten Christoffersen,

    1. Freshwater Biological Laboratory, University of Copenhagen, Helsingørsgade 51, DK-3400 Hillerød, Denmark.
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  • Brett A. Neilan

    Corresponding author
    1. School of Microbiology and Immunology, University of New South Wales, Sydney 2052, Australia.
      *For correspondence. E-mail b.neilan@unsw.edu.au; Tel. (+61) 2 9385 3235; Fax (+61) 2 9385 1591.
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*For correspondence. E-mail b.neilan@unsw.edu.au; Tel. (+61) 2 9385 3235; Fax (+61) 2 9385 1591.

Abstract

Microcystis aeruginosa strain MRC is unique in its' possession of the mcyA-J gene cluster, which encodes microcystin synthetase, but its' inability to produce microcystins. M. aeruginosa strain MRD is genetically identical to MRC at numerous genomic loci examined, but produces a variety of microcystins, mainly with the amino acid tyrosine in the molecule. Zooplankton studies with Daphnia galeata and D. pulicaria, using the mutant (MRC) and its' wild type (MRD), showed for the first time that microcystins other than microcystin-LR can be responsible for the poisoning of Daphnia by Microcystis. Regardless of microcystin content, both Daphnia exhibited significantly reduced ingestion rates when fed with either strain of M. aeruginosa compared with the green alga Scenedesmus acutus. A disruption of the molting process in both Daphnia spp. was noted when these species were fed with MRC cells. Such symptoms on Daphnia have not been previously reported for cyanobacteria and may point to a bioactive compound, other than microcystin, which inhibits the hardening of protein–chitin complexes in Daphnia.

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