Effect of low temperature on contributions of ammonia oxidizing archaea and bacteria to nitrous oxide in constructed wetlands

Constructed wetlands (CWs) have been widely used for ecological remediation of micro-polluted source water. Nitrous oxide (N2O) from CWs has caused great concern as a greenhouse gas. However, the contribution of ammonia oxidation driven by ammonia oxidizing archaea (AOA) and ammonia oxidizing bacteria (AOB) to N2O emission, especially at low temperature, was unknown. This study aimed to quantify the contributions of AOA and AOB to N2O through lab-scale subsurface CWs. The N2O emission flux of CW at 8 degrees C was 1.23 mg m(-2).h(-1), significantly lower than that at 25 degrees C (1.92 mg m(-2).h(-1)). The contribution of ammonia oxidation to N2O at 8 degrees C (33.04%) was significantly higher than that at 25 degrees C (24.17%). The N2O production from AOA increased from 1.91 ng N.g(-1) at 25 degrees C to 4.11 ng N.g(-1) soil at 8 degrees C and its contribution increased from 23.38% to 30.18% (P < 0.05). Low temperature impaired functional gene groups and inhibited the activity of AOB, resulting in its declined contribution. Based on the transcriptional analysis, AOA was less affected by low temperature, thus stably contributing to N2O. Moreover, community diversity and relationships of AOA were enhanced at 8 degrees C, while AOB declined. The results confirmed the significant contribution of AOA and demonstrated molecular mechanisms (higher activity and community stability) of the increased contribution of AOA to N2O at low temperature.

Automated summary

This study quantified the contributions of ammonia oxidizing archaea (AOA) and ammonia oxidizing bacteria (AOB) to nitrous oxide (N2O) emission through lab-scale subsurface constructed wetlands (CWs) at different temperatures. The results showed that AOA significantly contributed to N2O at low temperature, with higher activity and community stability compared to AOB. On the other hand, AOB's contribution declined due to low temperature inhibition.