4.6 Article

Fate of hepatotoxin microcystin during infection of cyanobacteria by fungal chytrid parasites

Journal

HARMFUL ALGAE
Volume 118, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.hal.2022.102288

Keywords

Cyanobacteria; Microcystin release; Microcystin upregulation; Chytridiomycota; Parasites; Bloom decay

Funding

  1. German Science Foundation (DFG)
  2. International IGB Fellowship Freshwater Science
  3. [AG 284/1-1]

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Chytrid parasites are recognized as effective control agents of cyanobacteria, but their infection does not lead to a significant increase in toxin production. This suggests that chytrid epidemics do not result in massive toxin release.
Chytrid parasites are increasingly recognized as ubiquitous and potent control agents of phytoplankton, including bloom-forming toxigenic cyanobacteria. In order to explore the fate of the cyanobacterial toxin microcystins (MCs) and assess potential upregulation of their production under parasite attack, a laboratory experiment was conducted to evaluate short-and long-term variation in extracellular and intracellular MC in the cyanobacteria Planktothrix agardhii and P. rubescens, both under chytrid infection and in the presence of lysates of previously infected cyanobacteria. MCs release under parasite infection was limited and not different to unin-fected cyanobacteria, with extracellular toxin shares never exceeding 10%, substantially below those caused by mechanical lysis induced by a cold-shock. Intracellular MC contents in P. rubescens under infection were not significantly different from uninfected controls, whereas infected P. agardhii showed a 1.5-fold increase in intracellular MC concentrations, but this was detected within the first 48 hours after parasite inoculation and not later, indicating no substantial MC upregulation in cells being infected. The presence of lysates of previously infected cyanobacteria did not elicit higher intracellular MC contents in exposed cyanobacteria, speaking against a putative upregulation of toxin production induced via quorum sensing in response to parasite attack. These results indicate that chytrid epidemics can constitute a bloom decay mechanism that is not accompanied by massive release of toxins into the medium.

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