Verdon Nia, Popescu Ofelia, Titmuss Simon, Allen Rosalind J
Theoretical Microbial Ecology, Institute of Microbiology, Faculty of Biological Sciences, Friedrich Schiller University, Jena, Germany.
Cluster of Excellence Balance of the Microverse, Friedrich Schiller University, Jena, Germany.
J R Soc Interface. 2025 Feb;22(223):20240611. doi: 10.1098/rsif.2024.0611. Epub 2025 Feb 12.
Microbes often inhabit complex, spatially partitioned environments such as host tissue or soil, but the effects of habitat fragmentation on microbial ecology and infection dynamics are poorly understood. Here, we investigate how habitat fragmentation impacts a prevalent microbial collective defence mechanism: enzymatic degradation of an environmental toxin. Using a theoretical model, we predict that habitat fragmentation can strongly enhance the collective benefits of enzymatic toxin degradation. For the example of [Formula: see text]-lactamase-producing bacteria that mount a collective defence by degrading a [Formula: see text]-lactam antibiotic, we find that realistic levels of habitat fragmentation can allow a population to survive antibiotic doses that greatly exceed those required to kill a non-fragmented population. This 'habitat-fragmentation rescue' is a stochastic effect that originates from variation in bacterial density among different subpopulations and demographic noise. We also study the contrasting case of collective enzymatic foraging, where enzyme activity releases nutrients from the environment; here we find that increasing habitat fragmentation decreases the lag time for population growth but does not change the ecological outcome. Taken together, this work predicts that stochastic effects arising from habitat fragmentation can greatly enhance the effectiveness of microbial collective defence via enzymatic toxin degradation.
微生物常常栖息于复杂的、空间上分隔的环境中,如宿主组织或土壤,但人们对栖息地破碎化对微生物生态和感染动态的影响却知之甚少。在这里,我们研究栖息地破碎化如何影响一种普遍的微生物集体防御机制:环境毒素的酶促降解。通过一个理论模型,我们预测栖息地破碎化能够显著增强酶促毒素降解的集体效益。以通过降解β-内酰胺抗生素进行集体防御的产β-内酰胺酶细菌为例,我们发现实际水平的栖息地破碎化能使种群在远超杀死非破碎化种群所需剂量的抗生素环境中存活。这种“栖息地破碎化拯救”是一种随机效应,源于不同亚种群间细菌密度的差异和种群统计学噪声。我们还研究了集体酶促觅食的相反情况,即酶活性从环境中释放养分;在此我们发现,增加栖息地破碎化会缩短种群增长的滞后时间,但不会改变生态结果。综上所述,这项研究预测,栖息地破碎化产生的随机效应能够通过酶促毒素降解极大地增强微生物集体防御的有效性。