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Lookup NU author(s): Professor Neil GrayORCiD,
Dr Jan DolfingORCiD
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND).
© 2021 The Author(s). Rice paddies are major contributors to anthropogenic greenhouse gas emissions via methane (CH4) flux. The accurate quantification of CH4 emissions from rice paddies remains problematic, in part due to uncertainties and omissions in the contribution of microbial aggregates on the soil surface to carbon fluxes. Herein, we comprehensively evaluated the contribution of one form of microbial aggregates, periphytic biofilm (PB), to carbon dioxide (CO2) and CH4 emissions from paddies distributed across three climatic zones, and quantified the pathways that drive net CH4 production as well as CO2 fixation. We found that PB accounted for 7.1%–38.5% of CH4 emissions and 7.2%–12.7% of CO2 fixation in the rice paddies. During their growth phase, PB fixed CO2 and increased the redox potential, which promoted aerobic CH4 oxidation. During the decay phase, PB degradation reduced redox potential and increased soil organic carbon availability, which promoted methanogenic microbial community growth and metabolism and increased CH4 emissions. Overall, PB acted as a biotic converter of atmospheric CO2 to CH4, and aggravated carbon emissions by up to 2,318 kg CO2 equiv ha−1 season−1. Our results provide proof-of-concept evidence for the discrimination of the contributions of surface microbial aggregates (i.e., PB) from soil microbes, and a profound foundation for the estimation and simulation of carbon fluxes in a potential novel approach to the mitigation of CH4 emissions by manipulating PB growth.
Author(s): Wang S, Sun P, Zhang G, Gray N, Dolfing J, Esquivel-Elizondo S, Peñuelas J, Wu Y
Publication type: Article
Publication status: Published
Journal: The Innovation
Print publication date: 25/01/2022
Online publication date: 26/11/2021
Acceptance date: 23/11/2021
Date deposited: 05/01/2022
ISSN (electronic): 2666-6758
Publisher: Cell Press
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