Hypoxia and acidification interact to disrupt nitrification and stimulate its nitrous oxide production in estuarine and coastal waters

The concurrent intensification of acidification and hypoxia poses a growing threat to estuarine and coastal ecosystems globally, yet their interactive impacts on nitrification, a key process in the nitrogen (N) cycle and a major source of nitrous oxide (N2O), remain poorly understood. In this study, using 15N isotope tracing, we demonstrated that the co-occurrence of acidification and hypoxia exerted an antagonistic interaction, suppressing nitrification rates while stimulating nitrification-derived N2O emissions to a lesser extent than the sum of their individual effects along the estuarine-coastal continuum. Metatranscriptomic analysis further elucidated the molecular underpinnings, revealing that both stressors downregulated key nitrification genes (e.g., ammonia monooxygenase gene, amoA) and upregulated N2O-producing genes (e.g., nitric oxide reductase gene, nor) in nitrifiers. It also revealed that nitrifiers employ a key coping strategy through transcriptional regulation of core cellular metabolism, involving genes for electron transport chain, proton pumping, and autotrophic carbon assimilation. Monte Carlo simulations estimated that acidification and hypoxia jointly drive a median global increase of 0.96 (IQR: 0.28–2.45) Tg N2O-N yr-1 in estuarine and coastal emissions. Collectively, these findings demonstrate that the global intensification of acidification and hypoxia could disrupt microbial N cycling and enhance N2O emissions, thereby intensifying coastal eutrophication and impeding climate mitigation.