Department of Plant and Microbial Biology, North Carolina State University, Raleigh, NC, USA.
Department of Biology, University of North Carolina Greensboro, Greensboro, NC, USA.
Genome Biol Evol. 2024 Aug 5;16(8). doi: 10.1093/gbe/evae149.
Opportunistic pathogens are environmental microbes that are generally harmless and only occasionally cause disease. Unlike obligate pathogens, the growth and survival of opportunistic pathogens do not rely on host infection or transmission. Their versatile lifestyles make it challenging to decipher how and why virulence has evolved in opportunistic pathogens. The coincidental evolution hypothesis postulates that virulence results from exaptation or pleiotropy, i.e. traits evolved for adaptation to living in one environment that have a different function in another. In particular, adaptation to avoid or survive protist predation has been suggested to contribute to the evolution of bacterial virulence (the training ground hypothesis). Here, we used experimental evolution to determine how the selective pressure imposed by a protist predator impacts the virulence and fitness of a ubiquitous environmental opportunistic bacterial pathogen that has acquired multidrug resistance: Serratia marcescens. To this aim, we evolved S. marcescens in the presence or absence of generalist protist predator, Tetrahymena thermophila. After 60 d of evolution, we evaluated genotypic and phenotypic changes by comparing evolved S. marcescens with the ancestral strain. Whole-genome shotgun sequencing of the entire evolved populations and individual isolates revealed numerous cases of parallel evolution, many more than statistically expected by chance, in genes associated with virulence. Our phenotypic assays suggested that evolution in the presence of a predator maintained virulence, whereas evolution in the absence of a predator resulted in attenuated virulence. We also found a significant correlation between virulence, biofilm formation, growth, and grazing resistance. Overall, our results provide evidence that bacterial virulence and virulence-related traits are maintained by selective pressures imposed by protist predation.
机会性病原体是通常无害但偶尔会引起疾病的环境微生物。与专性病原体不同，机会性病原体的生长和存活并不依赖于宿主感染或传播。它们多样的生活方式使得难以理解毒力是如何以及为何在机会性病原体中进化的。偶然进化假说假设毒力是由适应或多效性产生的，即适应在一种环境中生存的特征在另一种环境中具有不同的功能。特别是，避免或存活原生动物捕食的适应被认为有助于细菌毒力的进化（训练场假说）。在这里，我们使用实验进化来确定原生动物捕食者施加的选择压力如何影响一种普遍存在的环境机会性病原体的毒力和适应性，这种病原体已经获得了多药耐药性：粘质沙雷氏菌。为此，我们在有或没有普通原生动物捕食者嗜热四膜虫的情况下培养粘质沙雷氏菌。经过 60 天的进化，我们通过比较进化后的粘质沙雷氏菌与原始菌株来评估基因型和表型变化。对整个进化种群和单个分离株的全基因组鸟枪法测序揭示了许多与毒力相关的基因发生了平行进化，比随机情况下统计预期的要多得多。我们的表型测定表明，在捕食者存在的情况下进化保持了毒力，而在没有捕食者的情况下进化导致了毒力减弱。我们还发现毒力、生物膜形成、生长和抗捕食之间存在显著相关性。总体而言，我们的结果提供了证据，表明细菌毒力和与毒力相关的特征是由原生动物捕食施加的选择压力维持的。
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