Unraveling the mechanism of greenhouse gas emissions during allelochemical-triggered inhibition of cyanobacteria recovery.

Climate change amplifies cyanobacterial blooms, creating a feedback loop between warming and bloom intensity. This dynamic emphasizes the need to address greenhouse gas (GHG) emissions during in-situ cyanobacterial control, minimizing algicides use and its long-term climatic impacts. However, research on the dose-response of algicides on GHG emissions is limited. This study investigated the dose-dependent effects of artemisinin sustained-release algicides (ASAs) on GHG emissions and microbial dynamics during cyanobacteria recovery prevention. Microcosm experiments revealed that ASAs dosage reshaped the carbonate system, lowering pH and increasing DOC and C/N ratio, promoting short-term CO₂ emissions. Microbial diversity decreased with higher ASAs dosage, and Proteobacteria replaced Cyanobacteria as the dominant group. The formate metabolic pathway, which produces CO₂, was strengthened, while CH₄ oxidation was weakened. The abundance of genera such as Curvibacter, Burkholderiales, and Acetobacterales increased, correlating with enhanced carbon and nitrogen metabolism, while CH₄-oxidizing genera like Methylobacterium and Methylorubrum showed reduced abundance, associated with weakened CH₄ metabolism. Co-occurrence networks emphasized that the ASAs gradient indirectly affected dominant microbes and carbon-nitrogen metabolism by altering water chemistry. ASAs exacerbated GHG emissions by coupling environmental changes with microbial metabolism. Our findings provide a theoretical basis for using lower ASAs dose during cyanobacteria recovery prevention and underscore the importance of considering biogeochemical cycles and ecosystem impacts in cyanobacterial control.