@article{SchuurmansBrinkmannMakoweretal.2018, author = {Schuurmans, Jasper Merijn and Brinkmann, Bregje W. and Makower, Katharina and Dittmann, Elke and Huisman, Jef and Matthijs, Hans C. P.}, title = {Microcystin interferes with defense against high oxidative stress in harmful cyanobacteria}, series = {Harmful algae}, volume = {78}, journal = {Harmful algae}, publisher = {Elsevier}, address = {Amsterdam}, issn = {1568-9883}, doi = {10.1016/j.hal.2018.07.008}, pages = {47 -- 55}, year = {2018}, abstract = {Harmful cyanobacteria producing toxic microcystins are a major concern in water quality management. In recent years, hydrogen peroxide (H2O2) has been successfully applied to suppress cyanobacterial blooms in lakes. Physiological studies, however, indicate that microcystin protects cyanobacteria against oxidative stress, suggesting that H2O2 addition might provide a selective advantage for microcystin-producing (toxic) strains. This study compares the response of a toxic Microcystis strain, its non-toxic mutant, and a naturally non-toxic Microcystis strain to H2O2 addition representative of lake treatments. All three strains initially ceased growth upon H2O2 addition. Contrary to expectation, the non-toxic strain and non-toxic mutant rapidly degraded the added H2O2 and subsequently recovered, whereas the toxic strain did not degrade H2O2 and did not recover. Experimental catalase addition enabled recovery of the toxic strain, demonstrating that rapid H2O2 degradation is indeed essential for cyanobacterial survival. Interestingly, prior to H2O2 addition, gene expression of a thioredoxin and peroxiredoxin was much lower in the toxic strain than in its non-toxic mutant. Thioredoxin and peroxiredoxin are both involved in H2O2 degradation, and microcystin may potentially suppress their activity. These results show that microcystin-producing strains are less prepared for high levels of oxidative stress, and are therefore hit harder by H2O2 addition than non-toxic strains.}, language = {en} } @article{MakowerSchuurmansGrothetal.2015, author = {Makower, A. Katharina and Schuurmans, J. Merijn and Groth, Detlef and Zilliges, Yvonne and Matthijs, Hans C. P. and Dittmann-Th{\"u}nemann, Elke}, title = {Transcriptomics-Aided dissection of the intracellular and extracellular roles of microcystin in microcystis aeruginosa PCC 7806}, series = {Applied and environmental microbiology}, volume = {81}, journal = {Applied and environmental microbiology}, number = {2}, publisher = {American Society for Microbiology}, address = {Washington}, issn = {0099-2240}, doi = {10.1128/AEM.02601-14}, pages = {544 -- 554}, year = {2015}, abstract = {Recent studies have provided evidence for both intracellular and extracellular roles of the potent hepatotoxin microcystin (MC) in the bloom-forming cyanobacterium Microcystis. Here, we surveyed transcriptomes of the wild-type strain M. aeruginosa PCC 7806 and the microcystin-deficient Delta mcyB mutant under low light conditions with and without the addition of external MC of the LR variant (MC-LR). Transcriptomic data acquired by microarray and quantitative PCR revealed substantial differences in the relative expression of genes of the central intermediary metabolism, photosynthesis, and energy metabolism. In particular, the data provide evidence for a lower photosystem I (PSI)-to-photosystem II (PSII) ratio and a more pronounced carbon limitation in the microcystin-deficient mutant. Interestingly, only 6\% of the transcriptional differences could be complemented by external microcystin-LR addition. This MC signaling effect was seen exclusively for genes of the secondary metabolism category. The orphan polyketide synthase gene cluster IPF38-51 was specifically downregulated in response to external MC-LR under low light. Our data suggest a hierarchical and light-dependent cross talk of secondary metabolites and support both an intracellular and an extracellular role of MC in Microcystis.}, language = {en} }