Collapse of quorum sensing networks underlies low-temperature failure of ammonia oxidation

Low-temperature failure of ammonia oxidation poses a persistent challenge for wastewater treatment in cold regions. While conventional explanations focus on physiological inhibition of ammonia-oxidizing bacteria (AOB), this study reveals an overlooked mechanism: temperature-driven collapse of microbial communication networks mediated by acyl-homoserine lactones (AHLs). Cooling from 25 °C to 10 °C reduced extracellular AHLs by 97.7 %, due to a decline in AHL-producers and downregulation of synthesis genes. This quorum sensing disruption initiated a damaging cascade: reactive oxygen species surged by 75.2 %, inducing oxidative damage; concurrently, Nitrosomonas abundance decreased by 35.7 % and microbial network restructuring led to the competitive exclusion of AOB by other taxa. These effects collectively reduced specific ammonia oxidation activity (SAOA) by 71.7 %, with structural equation modeling identifying AHLs as the dominant direct regulator. Exogenous C8-HSL addition reversed these impacts, restoring SAOA by 59.3 %. The treatment increased AOB abundance by 17.6 %, upregulated the expression of amo and hao genes by 24.0 %-241.1 %, and reduced oxidative damage by 30.3 %. Our findings establish quorum sensing disruption as a key bottleneck in low-temperature nitrification and highlight C8-HSL as a restorative mediator. We propose bioaugmentation with cold-adapted AHL-producers as a sustainable strategy for nitrogen removal in cold climates.