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Deciphering the genetic basis of microcystin tolerance
Authors:Anke Schwarzenberger  Thomas Sadler  Susanne Motameny  Kamel Ben-Khalifa  Peter Frommolt  Janine Altmüller  Kathryn Konrad  Eric von Elert
Affiliation:.Cologne Biocenter, Aquatic Chemical Ecology, University of Cologne, Zuelpicher Str. 47b, 50674 Cologne, Germany ;.Cologne Center for Genomics, University of Cologne, Weyertal 115b, 50931 Cologne, Germany ;.RRZK, University of Cologne, Weyertal 121, 50931 Cologne, Germany ;.CECAD Cologne, University of Cologne, Robert-Koch-Str. 21, 50931 Cologne, Germany
Abstract:

Background

Cyanobacteria constitute a serious threat to freshwater ecosystems by producing toxic secondary metabolites, e.g. microcystins. These microcystins have been shown to harm livestock, pets and humans and to affect ecosystem service and functioning. Cyanobacterial blooms are increasing worldwide in intensity and frequency due to eutrophication and global warming. However, Daphnia, the main grazer of planktonic algae and cyanobacteria, has been shown to be able to suppress bloom-forming cyanobacteria and to adapt to cyanobacteria that produce microcystins. Since Daphnia’s genome was published only recently, it is now possible to elucidate the underlying molecular mechanisms of microcystin tolerance of Daphnia.

Results

Daphnia magna was fed with either a cyanobacterial strain that produces microcystins or its genetically engineered microcystin knock-out mutant. Thus, it was possible to distinguish between effects due to the ingestion of cyanobacteria and effects caused specifically by microcystins. By using RNAseq the differentially expressed genes between the different treatments were analyzed and affected KOG-categories were calculated. Here we show that the expression of transporter genes in Daphnia was regulated as a specific response to microcystins. Subsequent qPCR and dietary supplementation with pure microcystin confirmed that the regulation of transporter gene expression was correlated with the tolerance of several Daphnia clones.

Conclusions

Here, we were able to identify new candidate genes that specifically respond to microcystins by separating cyanobacterial effects from microcystin effects. The involvement of these candidate genes in tolerance to microcystins was validated by correlating the difference in transporter gene expression with clonal tolerance. Thus, the prevention of microcystin uptake most probably constitutes a key mechanism in the development of tolerance and adaptation of Daphnia. With the availability of clear candidate genes, future investigations examining the process of local adaptation of Daphnia populations to microcystins are now possible.

Electronic supplementary material

The online version of this article (doi:10.1186/1471-2164-15-776) contains supplementary material, which is available to authorized users.
Keywords:
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