Acetylacetone Interferes with Carbon and Nitrogen Metabolism of Microcystis aeruginosa by Cutting Off the Electron Flow to Ferredoxin

The regulation of photosynthetic machinery with a nonoxidative approach is a powerful but challenging strategy for the selective inhibition of bloom-forming cyanobacteria. Acetylacetone (AA) was recently found to be a target-selective cyanocide for Microcystis aeruginosa, but the cause and effect in the studied system are still unclear. By recording of the chemical fingerprints of the cells at two treatment intervals (12 and 72 h with 0.1 mM AA) with omics assays, the molecular mechanism of AA in inactivating Microcystis aeruginosa was elucidated. The results clearly reveal the effect of AA on ferredoxin and the consequent effects on the physiological and biochemical processes of Microcystis aeruginosa. In addition to its role as an electron acceptor of photosystem I, ferredoxin plays pivotal roles in the assimilation of nitrogen in cyanobacterial cells. The effect of AA on ferredoxin and on nonheme iron of photosystem II first cut off the photosynthetic electron transfer flow and then interrupted the synthesis of adenosine triphosphate (ATP) and reduced nicotinamide adenine dinucleotide phosphate (NADPH), which ultimately might affect carbon fixation and nitrogen assimilation metabolisms. The results here provide missing pieces in the current knowledge on the selective inhibition of cyanobacteria, which should shed light on the better control of harmful blooms.