Methane (CH4) is a potent greenhouse gas that accounts for approximately 20–30% of global warming, second only to carbon dioxide (CO2). Consequently, it is one of the leading targets in short-term global warming mitigation. The only known natural way to filter methane are by methane-oxidising bacteria (methanotrophs). Protists such as amoebae and ciliates have been recognised as grazers of methanotrophs. Yet, the interplay between nutrient stress, especially phosphorus, an essential macronutrient for bacterial activity, and methanotroph susceptibility to predation is poorly characterised.

Recent research has reported that methanotrophs such as Methylosinus trichosporium OB3b can remodel their membrane lipids in P-deficient conditions by replacing phospholipids with glycolipids. However, the ecological role of this process, in particular, resistance or susceptibility to protozoan predation, is still unknown, while global warming is expected to exacerbate nutrient deficiencies in surface waters. We hypothesise that phosphorus-driven lipid remodelling in methanotrophs influences their susceptibility to protist predation, altering predator-prey dynamics and impacting methane oxidation in nutrient-limited environments.

To test this, we will use a variety of interaction experiments to observe the ingestion, growth, and digestion of prey inside protozoa predators. In addition, this study focuses on methanotrophs in greater depth by examining membrane lipid remodelling of different strains in phosphorus-limited conditions using LC/MS.

By gaining a greater understanding of methanotrophic bacteria and their trade-off mechanisms in nutrient-limited conditions, this research seeks to predict how these limitations modify the bacterial membrane, predation by heterotrophic protists and ultimately their ability to oxidize methane.