Schwarzenberger, Anke, Sadler, Thomas ORCID: 0000-0002-8621-379X, Motameny, Susanne, Ben-Khalifa, Kamel, Frommolt, Peter ORCID: 0000-0002-1966-8014, Altmueller, Janine, Konrad, Kathryn and von Elert, Eric ORCID: 0000-0001-7758-716X (2014). Deciphering the genetic basis of microcystin tolerance. BMC Genomics, 15. LONDON: BMC. ISSN 1471-2164

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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.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Schwarzenberger, AnkeUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Sadler, ThomasUNSPECIFIEDorcid.org/0000-0002-8621-379XUNSPECIFIED
Motameny, SusanneUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ben-Khalifa, KamelUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Frommolt, PeterUNSPECIFIEDorcid.org/0000-0002-1966-8014UNSPECIFIED
Altmueller, JanineUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Konrad, KathrynUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
von Elert, EricUNSPECIFIEDorcid.org/0000-0001-7758-716XUNSPECIFIED
URN: urn:nbn:de:hbz:38-428850
DOI: 10.1186/1471-2164-15-776
Journal or Publication Title: BMC Genomics
Volume: 15
Date: 2014
Publisher: BMC
Place of Publication: LONDON
ISSN: 1471-2164
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
DAPHNIA-MAGNA; PROTEASE INHIBITORS; LOCAL ADAPTATION; TOXIC CYANOBACTERIUM; EXPRESSION; AERUGINOSA; RESISTANCE; GENOMICS; GROWTH; IDENTIFICATIONMultiple languages
Biotechnology & Applied Microbiology; Genetics & HeredityMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/42885

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