Black Katrina A, Nguyen Julie V, Ramsey Jolene R, Tovey Jack C, Cameron Daniel L, Alexandrovics Jack, Glukhova Alisa, Papenfuss Anthony T, Call Melissa J, Young Ryland, Call Matthew E
The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.
Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia.
Mol Biotechnol. 2025 Jun 3. doi: 10.1007/s12033-025-01453-1.
Bacteriophage contaminations pose substantial risks to biomolecular production pipelines, and their resolution is especially difficult when the identity of the offending agent is unknown. We recently experienced an outbreak of Escherichia coli culture lysis in our Melbourne-based structural biology labs that halted protein production despite our use of T1-resistant (TonA/FhuA-disrupted) strains. Genetic analysis of the isolated phage yielded a 45,053 bp genome showing 80-90% identity with multiple Rtp-like siphophages, and transmission electron microscopy images were consistent with this classification. Further analysis revealed that our isolate was nearly identical to a highly virulent lytic coliphage MSK, recently isolated in Hangzhou, China, whose host receptor has not been determined. Sequence and structural modelling analysis of its putative receptor-binding protein suggested that its terminal receptor was likely to be LptD, an essential outer membrane protein involved in lipopolysaccharide transport. Based on a recent report of spontaneously arising mutations that blocked infection by other LptD-dependent bacteriophages, we designed a targeted genomic LptD loop deletion that successfully generated resistance to vB_EcoS_OzMSK in E. coli BL21(DE3) without apparent detriment to fitness. Here, we report a CRISPR-based, single-plasmid solution that will benefit other labs or facilities experiencing challenges due to LptD-dependent lytic phage outbreaks.
噬菌体污染对生物分子生产流程构成重大风险,当致病因子身份不明时,解决污染问题尤其困难。我们墨尔本的结构生物学实验室最近发生了一起大肠杆菌培养物裂解事件,尽管我们使用了抗T1(TonA/FhuA缺失)菌株,但蛋白质生产仍被迫中断。对分离出的噬菌体进行基因分析,得到了一个45,053 bp的基因组,与多种Rtp样肌尾噬菌体有80-90%的同源性,透射电子显微镜图像也与该分类结果一致。进一步分析表明,我们分离出的噬菌体与最近在中国杭州分离出的一种高毒力裂解性大肠杆菌噬菌体MSK几乎相同,其宿主受体尚未确定。对其假定的受体结合蛋白进行序列和结构建模分析表明,其末端受体可能是LptD,这是一种参与脂多糖转运的必需外膜蛋白。基于最近一份关于自发产生的突变可阻止其他依赖LptD的噬菌体感染的报告,我们设计了一种靶向基因组LptD环缺失方法,成功地在大肠杆菌BL21(DE3)中产生了对vB_EcoS_OzMSK的抗性,且对其适应性无明显损害。在此,我们报告一种基于CRISPR的单质粒解决方案,这将使其他因依赖LptD的裂解性噬菌体爆发而面临挑战的实验室或设施受益。