The control of harmful cyanobacterial blooms has been becoming a global challenge. The development of eco-friendly algicides with strong specificity is urgently needed. The photosynthetic apparatus is a promising target site for algicides to minimize the possible harmful effects on animals and humans. In this study, biologically derived 2-hydroxychalcone efficiently inhibited the growth of bloom-forming M. aeruginosa by selectively interfering with photosynthesis. 2-Hydroxychalcone targeting Photosystem II (PSII) inhibited electron transfer between the primary and secondary electron acceptors (QA and QB) and the binding of plastoquinone (PQ) molecules to the QB binding pocket at the acceptor side of PSII, as revealed by polyphasic chlorophyll (Chl) a fluorescence induction and QA- reoxidation kinetics. Molecular docking for 2-hydroxychalcone to D1 protein and the proteomic responses of M. aeruginosa suggested that 2-hydroxychalcone formed a stable monodentate ligand with the nonheme iron in D1 protein, provoking significant modulation of PSII proteins. The unique binding mode of 2-hydroxychalcone with PSII differentiated it from classical PSII inhibitors. Furthermore, 2-hydroxychalcone down-regulated the expression of microcystin (MC) synthesis-related genes to restrain MC synthesis and release. These results indicated the potential application of 2-hydroxychalcone as an algicide or a template scaffold for designing novel derivatives with superior algicidal activity.
Keywords: 2-hydroxychalcone; Microcystis aeruginosa; algicide; cyanobacterial bloom; photosynthesis inhibitor.