Institute of Molecular Biosciences, University of Graz, Graz, Austria.
Institute of Molecular Biosciences, University of Graz, Graz, Austria
mSphere. 2018 May 23;3(3). doi: 10.1128/mSphereDirect.00238-18. eCollection 2018 May-Jun.
During its life cycle, the facultative human pathogen , which is the causative agent of the diarrheal disease cholera, needs to adapt to a variety of different conditions, such as the human host or the aquatic environment. Importantly, cholera infections originate from the aquatic reservoir where persists between the outbreaks. In the aquatic environment, bacteria are constantly threatened by predatory protozoa and nematodes, but our knowledge of the response pathways and adaptation strategies of to such stressors is limited. Using a temporally controlled reporter system of transcription, we identified more than 100 genes of induced upon exposure to the nematode , which emerged recently as a valuable model for environmental predation during the aquatic lifestyle of Besides others, we identified and validated the genes encoding the mannose-sensitive hemagglutinin (MSHA) type IV pilus to be significantly induced upon exposure to the nematode. Subsequent analyses demonstrated that the mannose-sensitive hemagglutinin is crucial for attachment of in the pharynx of the worm and initiation of colonization, which results in growth retardation and developmental delay of Thus, the surface adhesion factor MSHA could be linked to a fitness advantage of upon contact with bacterium-grazing nematodes. The waterborne diarrheal disease cholera is caused by the bacterium The facultative human pathogen persists as a natural inhabitant in the aquatic ecosystem between outbreaks. In contrast to the human host, requires a different set of genes to survive in this hostile environment. For example, predatory micrograzers are commonly found in the aquatic environment and use bacteria as a nutrient source, but knowledge of the interaction between bacterivorous grazers and is limited. In this study, we successfully adapted a genetic reporter technology and identified more than 100 genes activated by upon exposure to the bacterium-grazing nematode This screen provides a first glimpse into responses and adaptational strategies of the bacterial pathogen against such natural predators. Subsequent phenotypic characterization revealed the mannose-sensitive hemagglutinin to be crucial for colonization of the worm, which causes developmental delay and growth retardation.
在其生命周期中,兼性人类病原体,即引起腹泻病霍乱的病原体,需要适应各种不同的条件,如人类宿主或水生环境。重要的是,霍乱感染源自水生储层,该储层在暴发之间持续存在。在水生环境中,细菌不断受到捕食性原生动物和线虫的威胁,但我们对霍乱弧菌应对此类胁迫的反应途径和适应策略的了解有限。使用转录的时间控制报告系统,我们鉴定了超过 100 个霍乱弧菌在暴露于线虫时诱导的基因,线虫最近成为霍乱弧菌水生生活方式中环境捕食的有价值模型。除其他外,我们鉴定并验证了编码甘露糖敏感血凝素 (MSHA) 型 IV 菌毛的基因在暴露于线虫时显著诱导。随后的分析表明,甘露糖敏感血凝素对于在蠕虫的咽部附着和定植的起始至关重要,这导致霍乱弧菌的生长迟缓和发育延迟。因此,表面粘附因子 MSHA 可与霍乱弧菌接触细菌吞噬线虫时的适应性优势相关。 食源性腹泻病霍乱是由细菌引起的。兼性人类病原体在暴发之间作为水生生态系统中的天然居民持续存在。与人类宿主不同,霍乱弧菌需要一组不同的基因来在这种恶劣环境中生存。例如,捕食性微食者通常存在于水生环境中,并将细菌用作营养源,但对食菌性掠食者与霍乱弧菌之间的相互作用知之甚少。在这项研究中,我们成功地适应了遗传报告技术,并鉴定了超过 100 个霍乱弧菌在暴露于食菌性线虫时激活的基因。该筛选首次提供了对细菌病原体针对此类天然捕食者的反应和适应策略的了解。随后的表型特征表明甘露糖敏感血凝素对于蠕虫的定植至关重要,这会导致发育延迟和生长迟缓。