| Summary: | Thesis (Ph.D.)--University of Washington, 2019 The largest natural source of CH4 to the atmosphere is wetlands, which produce 20% to 50% of total global emissions. Vascular plants play a key role regulating wetland CH4 emissions through multiple mechanisms. They often contain aerenchymatous tissues which act as a diffusive pathway for CH4 to travel from the anoxic soil to the atmosphere and for O2 to diffuse into the soil and enable methanotrophy. Plants also exude carbon from their roots which stimulates microbial activity and fuels methanogenesis. This study investigated these mechanisms in a laboratory experiment utilizing rootboxes containing either Carex aquatilis plants, silicone tubes that simulated aerenchymatous gas transfer, or only soil as a control. The results are presented in three parts: the output of an isotope mixing model (Chapter 2), a mass spectroscopy investigation of changes caused to chemical composition of soil compounds (Chapter 3), and a metagenomic study of changes to the microbial ecosystem (Chapter 4). Chapter 2 shows that CH4 emissions were far greater from planted boxes than from control boxes or simulated plants, indicating that the physical transport pathway of aerenchyma was of little importance when not paired with other effects of plant biology. Plants were exposed to 13CO2 at two time-points and subsequent enrichment of root tissue, rhizosphere soil, and emitted CH4 was used in an isotope mixing model to determine the proportion of plant-derived versus soil-derived carbon supporting methanogenesis. Results showed that carbon exuded by plants was converted to CH4 but that plants also increased emission of soil-derived carbon relative to the other experimental treatments. This result signifies that plants and root exudates altered the soil chemical environment and microbial community such that microbial utilization of soil carbon was increased (e.g. microbial priming) and/or oxidation of soil-derived CH4 was decreased (e.g., by microbial competition for oxygen). Chapter 3 ...
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