Exploring an Efficient and Eco-Friendly Signaling Molecule and Its Quorum Quenching Ability for Controlling Microcystis Blooms

Cyanobacterial Blooms Formation by Enhanced Ecological Adaptability and Competitive Advantage of <em>Microcystis</em>— Non-Negligible Role of Quorum-Sensing

“…Microcystis strain AHLs homologs Culture medium [24] M. aeruginosa FACHB-905 AHLs(C12H17O5N) BG-11 [28] M. aeruginosa PCC7820 C8 HSLs Allen-BG11 [40] M. aeruginosa PCC-7820 AHLs(C12H17O5N) BG-11 [41] M. aeruginosa HB 836 3-OXO-C5-HSL BG-11 C6-HSL BG-11…”

“…For instance, Yan et al identified 3OH-C4-HSL (a AHL homolog) as QS signaling molecule of Microcystis, and verified that the addition of 3OH-C4-HSL could up-regulate QS-related genes Dpp and Sec, and the expression of genes related to NADH dehydrogenase, succinate dehydrogenase, cytochrome coxidase were also up-regulated to promote all ATP-synthesizing genes expression. Consequently, carbon and energy metabolisms were promoted in Microcystis [41]. This suggested that some AHLs homologs acted as the trigger to initiate a series of downstream metabolisms.…”

“…The premise of exploring exogenous AHLs function is that these AHLs produced by other organisms can affect Microcystis. Yan et al found that the addition of 3-OH-C4-HSL extracted from bacterial sludge could promote microalgal growth, alike to the function of endogenous AHLs [41], whereas Xue et al found that exogenous AHLs addition decreased Microcystis growth rate [62]. Based on numerous studies, exogenous AHLs affect Microcystis in several aspects alike to endogenous AHLs.…”

“…Researchers also revealed that a variety of plant-originated and synthetic organic compounds could serve as QS inhibitors, such as vanillin extracted from vanilla bean and a heterocyclic oxygenic compound named furan [28,41,69]. Zhai et al found that one of the furanone, dihydro-3-amino-2-(3H)-furanone (FN) and Microcystis's QS signaling molecule could bind to the same site on receptor [40].…”

“…Further research reported that FN could bind with such two residues as Asn164 (A) and His167 (A) of AHLs receptor LuxR to form hydrogen bonds. The hydrophobic interactions between FN and binding pockets formed by residues Gln137(A), Val140-(A), Ala163(A), Asn164(A) and His167(A) also enables FN to have more competitive advantage in receptor-binding than QS signal [41]. Such advantage effectively inhibited carbon assimilation and energy metabolism of Microcystis to control its cell density.…”