An integrated ecophysiology and omics study of phosphorus limitation in methane-oxidising bacteria (EcoMethane)
Lead Research Organisation:
University of Birmingham
Department Name: Sch of Biosciences
Abstract
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
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
