An integrated ecophysiology and omics study of phosphorus limitation in methane-oxidising bacteria (EcoMethane)

甲烷是一种强有力的大气温室气体，其浓度在过去十年中持续上升，导致最近在格拉斯哥举行的COP26全球会议努力到2030年将甲烷排放量减少30%。甲烷氧化菌(甲烷氧化菌)利用甲烷作为碳和能源，帮助减少多达90%的甲烷排放。因此，甲烷氧化菌在全球甲烷循环中扮演着至关重要的角色，自然环境中甲烷氧化菌活动的任何干扰，无论是生物的还是非生物的，都将对我们到2030年将全球变暖限制在1.5摄氏度的能力产生重大影响。然而，人们对现实世界中甲烷菌活性是如何调节的知之甚少，特别是受到磷(P)等关键营养物质的调控，磷是许多生态系统中限制植物和微生物生长的一种限制性营养物质。以甲氧西林天花粉OB3b为模型，用替代的非磷替代糖脂替代细胞膜磷脂，证明了甲氧菌可以通过替代膜磷脂来减少细胞对磷的限制。这种所谓的脂质重塑途径中涉及的基因在所有蛋白细菌甲烷氧化细菌中都是严格保守的，这表明脂质重塑是甲烷氧化细菌的一种保守特征。然而，这种对磷限制的适应的生态和生理后果尚不清楚。这一点很重要，因为它可能会对甲烷养殖者的活动和死亡率(甲烷养殖者与原生动物食草动物和噬菌体的生物相互作用)产生重要影响，从而影响全球甲烷收支。在这里，我的目标是用一种集成的组学方法来揭示甲烷氧化细菌的生态生理学以及它们在模式甲烷氧化细菌和它们的自然栖息地对磷限制的反应。该项目的成果将填补我们在理解自然环境中甲烷菌活动方面的一个主要知识空白。

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 abilityto limit global warming by 1.5 degrees celsius by 2030. However, very little is known about how methanotroph activity isregulated in the real world, particularly by key nutrients like phosphorus (P), a limiting nutrient constraining plantand microbial growth in many ecosystems. Using Methylosinus trichosporium OB3b as the model, I havedemonstrated that methanotrophs can reduce their cellular P quota in response to P limitation by substitutingmembrane phospholipids with alternative non-P surrogate glycolipids. The genes involved in this so-called lipidremodelling pathway are strictly conserved in all proteobacterial methanotrophs, suggesting that lipid remodellingis a conserved trait in methanotrophs. However, the ecological and physiological consequences of such anadaptation to P limitation are unknown. This is important because it may have important consequences formethanotroph 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 theecophysiology of methanotrophs and their response to P limitation in both model methanotrophs and in their naturalhabitat. The outcomes of this project will fill a major knowledge gap in our understanding of methanotroph activityin the natural environment