Methane-eating bacteria in soils and water consume up to 90% of methane emissions before they reach the atmosphere, but scientists don't know how a shortage of phosphorus—a common nutrient limit in many ecosystems—slows them down. This matters because methane is a potent greenhouse gas, and the world has pledged to cut emissions 30% by 2030. If phosphorus scarcity reduces methanotroph activity, natural methane consumption could drop, undermining those targets. The researcher has already shown that these bacteria can swap phosphorus-rich membrane fats for phosphorus-free substitutes when phosphorus is scarce, but the consequences for their growth, survival, and vulnerability to predators or viruses remain unknown. This project will use genetic and molecular techniques to track how model methanotrophs and wild populations respond to phosphorus limitation. The work is fundamental science: it fills a major gap in understanding what controls methane-eating bacteria in the real world. A clearer picture of these constraints could eventually improve methane budget models used by climate policymakers, or guide land management practices that maintain healthy methanotroph communities in wetlands, rice paddies, and landfills.
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Methane is a potent atmospheric greenhouse gas with concentrations continuing to increase in the past decade, leading to a recent global effort at COP26 in Glasgow to reduce methane emissions by 30% by 2030. Methane- oxidising bacteria (methanotrophs) use methane as a carbon and energy source, helping to mitigate as much as 90% of methane emissions. As such, methanotrophs play a vital role in the global methane cycle and any disturbance, biotic or abiotic, of methanotroph activity in the natural environment would exert significant impacts on our ability to limit global warming by 1.5 degrees celsius by 2030. However, very little is known about how methanotroph activity is regulated in the real world, particularly by key nutrients like phosphorus (P), a limiting nutrient constraining plant and microbial growth in many ecosystems. Using Methylosinus trichosporium OB3b as the model, I have demonstrated that methanotrophs can reduce their cellular P quota in response to P limitation by substituting membrane phospholipids with alternative non-P surrogate glycolipids. The genes involved in this so-called lipid remodelling pathway are strictly conserved in all proteobacterial methanotrophs, suggesting that lipid remodelling is a conserved trait in methanotrophs. However, the ecological and physiological consequences of such an adaptation to P limitation are unknown. This is important because it may have important consequences for methanotroph activity and mortality (biotic interactions of methanotrophs with protist grazers and bacteriophages), thus affecting the global methane budget. Here, I aim to use an integrated omics approach to uncover the ecophysiology of methanotrophs and their response to P limitation in both model methanotrophs and in their natural habitat. The outcomes of this project will fill a major knowledge gap in our understanding of methanotroph activity in the natural environment
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