Araujo-Garrido Juan Luis, Bernal-Bayard Joaquín, Ramos-Morales Francisco
Departamento de Genética, Facultad de Biología, Universidad de Sevilla, 41012 Sevilla, Spain.
Microorganisms. 2020 Mar 2;8(3):357. doi: 10.3390/microorganisms8030357.
Type III secretion systems are used by many Gram-negative bacterial pathogens to inject proteins, known as effectors, into the cytosol of host cells. These virulence factors interfere with a diverse array of host signal transduction pathways and cellular processes. Many effectors have catalytic activities to promote post-translational modifications of host proteins. This review focuses on a family of effectors with glycosyltransferase activity that catalyze addition of -acetyl-d-glucosamine to specific arginine residues in target proteins, leading to reduced NF-κB pathway activation and impaired host cell death. This family includes NleB from , NleB1 and NleB2 from enteropathogenic and enterohemorrhagic , and SseK1, SseK2, and SseK3 from . First, we place these effectors in the general framework of the glycosyltransferase superfamily and in the particular context of the role of glycosylation in bacterial pathogenesis. Then, we provide detailed information about currently known members of this family, their role in virulence, and their targets.
许多革兰氏阴性细菌病原体利用III型分泌系统将被称为效应蛋白的蛋白质注入宿主细胞的细胞质中。这些毒力因子会干扰多种宿主信号转导途径和细胞过程。许多效应蛋白具有催化活性,可促进宿主蛋白的翻译后修饰。本综述聚焦于一类具有糖基转移酶活性的效应蛋白,它们催化将N-乙酰-D-葡萄糖胺添加到靶蛋白中的特定精氨酸残基上,从而导致NF-κB途径激活减少和宿主细胞死亡受损。这个家族包括鼠伤寒沙门氏菌的NleB、肠致病性大肠杆菌和肠出血性大肠杆菌的NleB1和NleB2,以及鼠伤寒沙门氏菌的SseK1、SseK2和SseK3。首先,我们将这些效应蛋白置于糖基转移酶超家族的一般框架中,以及糖基化在细菌致病机制中的特定背景下。然后,我们提供有关该家族目前已知成员的详细信息、它们在毒力中的作用及其靶标。