亚抑菌浓度抗生素促进稻田产甲烷的电微生物学机制

抗生素通过抑制微生物活性从而限制甲烷产生, 但关键因素却在于其浓度。最新发现，亚抑菌浓度抗生素作为信号分子促进电活性生物膜形成和胞外电子传递能力，因而很可能反过来促进甲烷产生，但相关研究目前尚属空白。本项目拟以华南红壤稻田为研究对象，四环素、环丙沙星和磺胺甲恶唑等污染水稻土常见抗生素为模式物，以亚抑菌浓度抗生素促进电活性生物电子传递能力为切入点，运用光谱电化学、生物电化学工作站、DNA-SIP和多组学测序等多种生物电化学和分子手段，系统研究亚抑菌浓度抗生素调控电活性生物膜电子传递能力的信号分子机制，探明电活性微生物胞外及种间电子传递过程对抗生素信号分子作用的响应及对产甲烷的影响效应，解析参与种间直接电子传递的产甲烷功能种群及互作机制。本研究将进一步拓展抗生素影响稻田微生物胞外及种间电子传递机制和产甲烷效应的认知，为合理评估污染稻田的温室气体排放提供科学依据和理论支撑。

Antibiotics inhibit the methanogenesis due to the restricting of microorganisms activity, in which the concentration of antibiotics play an important role. Recently, as signaling molecules, anbitiotics with subinhibitory concentrations (sub-MIC) were demonstrated to stimulate the increase of electro active biofilm and the ability of extracellular electron transfer (EET) of electromicroorganism, which could reversely facilitate the methanogenesis. However, less attention has been paid to the influence of antibiotics with subinhibitory concentrations on methanogenesis in rice paddy soils. Therefore, in this project, based on the EET ability stimulated by antibiotics with sub-MIC, using paddy soils of South China, and tetracycline, ciprofloxacin， and sulfamethoxazole as the typical antibiotics, we will employ the spectraelectrochemistry, bioelectrochemical systems, DNA-SIP, and multi-omics to explore the syntrophic metabolism between electromicroorganisms and methanogens. Moreover, we will investigate the ability of EET and interspecies electron transfer driven by electromicrooganisms responded to antibiotics with sub-MIC, and the key microoganisms involved in DIET to reveal the influence of antibiotics with sub-MIC on methanogenesis in paddy soils. We hope that the results of this project can provide new insight into understanding of EET and DIET in paddy soils impacted by antibiotics, and offer theoretical foundation for the estimation of greenhouse gas emission of paddy soil polluted by antibiotics.