Mocăniță Mădălina, Martz Kailey, D'Costa Vanessa M
Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Centre for Infection, Immunity and Inflammation, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Commun Biol. 2025 Apr 10;8(1):597. doi: 10.1038/s42003-025-07950-y.
Bacterial pathogens have evolved diverse strategies to manipulate host cells to establish infection. At a molecular level, this is often mediated by virulence factors that are secreted into host cells (herein referred to as effectors), which target host cellular pathways by initiating host-pathogen protein-protein interactions that alter cellular function in the host. By establishing this network of host-pathogen protein-protein interactions, pathogenic bacteria modulate and hijack host cell processes for the benefit of the pathogen, ultimately promoting survival, replication, and cell-to-cell spread within the host. Effector proteins also mediate diverse host-microbe interactions in nature, contributing to symbiotic relationships spanning from mutualism to commensalism to parasitism. While effector proteins play crucial roles in nature, molecular properties such as the transient nature of the underlying protein-protein interactions and their affinity for targeting host biological membranes often presents challenges to elucidating host targets and mechanism of action. Proximity-dependent biotin identification (termed BioID) has proven to be a valuable tool in the field of cell biology to identify candidate protein-protein interactions in eukaryotic cells, yet has remained relatively underexploited by bacterial pathogenesis researchers. Here, we discuss bacterial effector function at a molecular level, and challenges presented by traditional approaches to host target identification. We highlight the BioID approach and its potential strengths in the context of identifying host-pathogen protein-protein interactions, and explore BioID's implementation to study host-microbe interactions mediated by bacteria. Collectively, BioID represents a powerful tool for the study of bacterial effector proteins, providing new insight into our understanding of pathogenesis and other symbiotic relationships, and opportunities to identify new factors that contribute to host response to infection.
细菌病原体已经进化出多种策略来操纵宿主细胞以建立感染。在分子水平上,这通常由分泌到宿主细胞中的毒力因子(本文中称为效应子)介导,这些效应子通过启动宿主 - 病原体蛋白质 - 蛋白质相互作用来靶向宿主细胞途径,从而改变宿主细胞的功能。通过建立这种宿主 - 病原体蛋白质 - 蛋白质相互作用网络,病原菌调节并劫持宿主细胞过程以利于病原体,最终促进其在宿主体内的存活、复制和细胞间传播。效应蛋白在自然界中还介导多种宿主 - 微生物相互作用,有助于从互利共生到共生再到寄生的共生关系。虽然效应蛋白在自然界中发挥着关键作用,但诸如潜在蛋白质 - 蛋白质相互作用的短暂性质及其对靶向宿主生物膜的亲和力等分子特性,常常给阐明宿主靶点和作用机制带来挑战。邻近依赖性生物素识别(称为BioID)已被证明是细胞生物学领域中用于识别真核细胞中候选蛋白质 - 蛋白质相互作用的有价值工具,但在细菌致病机制研究人员中相对未得到充分利用。在这里,我们在分子水平上讨论细菌效应子功能以及传统宿主靶点识别方法所面临的挑战。我们强调BioID方法及其在识别宿主 - 病原体蛋白质 - 蛋白质相互作用方面的潜在优势,并探讨BioID在研究细菌介导的宿主 - 微生物相互作用中的应用。总的来说,BioID是研究细菌效应蛋白的有力工具,为我们理解发病机制和其他共生关系提供了新的见解,并有机会识别有助于宿主对感染作出反应的新因素。