Physiological interaction of Daphnia and Microcystis with regard to cyanobacterial secondary metabolites

• We investigate the Daphnia–cyanobacteria interaction on a physiological level.
• None of seven investigated metabolites is biotransformed by Daphnia.
• The cyanobacterial metabolites are exported out of Daphnia tissue instead.
• Our data suggest the presence of new inducible defence mechanisms in cyanobacteria.

Cyanobacterial blooms in freshwater ecosystems are a matter of high concern with respect to human health and ecosystem services. Investigations on the role of cyanobacterial secondary metabolites have largely been confined to microcystins, although cyanobacteria produce a huge variety of toxic or inhibitory secondary metabolites. Mass occurrences of toxic cyanobacteria strongly impact freshwater zooplankton communities; especially the unselective filter feeder Daphnia. Daphnids have been shown to successfully suppress bloom formation. However, the opposite situation, i.e. the suppression of Daphnia populations by cyanobacteria can be observed as well. To understand these contradictory findings the elucidation of the underlying physiological mechanisms that help daphnids to cope with cyanotoxins is crucial.We fed Daphnia magna with the cyanobacterium Microcystis aeruginosa PCC7806 for 24 h and used high-resolution LCMS analytics to analyze the Microcystis cells, the Daphnia tissue and the surrounding medium in order to investigate the fate of seven investigated cyanobacterial compounds (cyanopeptolins A–C, microcyclamide 7806A and aerucyclamides B–D). For none of these bioactive compounds evidence for biotransformation or biodegradation by Daphnia were found. Instead feeding and subsequent release experiments point at the importance of transport mechanisms in Daphnia with regard to the cyanopeptolins A and C and microcyclamide 7806A.In addition we found hints for new inducible defense mechanism in Microcystis against predation by Daphnia. These putative defense mechanisms include the elevated production of toxic compounds other than microcystins, as could be demonstrated here for aerucyclamide B and D, cyanopoeptolin B and microcyclamide 7806A. Moreover, our data demonstrate the elevated active export of at least one cyanobacterial compound (microcyclamide 7806A) into the surrounding medium as a response to grazer presence, which might constitute an entirely new not yet described cyanobacterial defense mechanism.