细菌水解NAD^(+)抵御噬菌体感染的机制研究进展  

Progress in the Study of the Mechanism by Which Bacteria Hydrolyze of NAD^(+) to Defend Against Bacteriophage Infection

作　　者：吴书娴 张丹丹 甄向凯 WU Shuxian;ZHANG Dandan;ZHEN Xiangkai(College of Life Sciences,Fujian Normal University,Fuzhou 350117,China)

机构地区：[1]福建师范大学生命科学学院,福建福州350117

出　　处：《福建师范大学学报(自然科学版)》2025年第1期95-101,共7页Journal of Fujian Normal University:Natural Science Edition

基　　金：国家自然科学基金项目(821700145);福建省中青年教师教育科研项目(JAT220048)。

摘　　要：在长期的进化过程中,细菌利用CRISPR-Cas系统、限制-修复等免疫系统对抗噬菌体的感染。近年几十个新颖的抗噬菌体系统被发现,其普遍机制为通过极其多样的方式使被感染的细胞死亡或代谢停滞,以阻止噬菌体的进一步扩增。目前研究表明,噬菌体的感染能激活具有NAD^(+)水解酶功能的效应蛋白,触发NAD^(+)的快速水解。并总结了新发现的水解NAD^(+)发挥抗噬菌体入侵的效应蛋白的分子机制,为病原菌的防治以及开发高效噬菌体制剂提供理论和新视角。Over the course of long-term evolution,bacteria have employed CRISPR-Cas systems,restriction-modification,and other immune systems to combat phage infections.In recent years,dozens of novel anti-phage systems have been identified,with a common mechanism that induces the death or metabolic stasis of infected cells through highly diverse ways,thereby preventing the further amplification of phages.Current studies have shown that phage infection can activate effector proteins with NAD^(+) hydrolase function,triggering rapid hydrolysis of NAD^(+).This review summarizes the molecular mechanisms of newly discovered effector proteins that hydrolyze NAD^(+) to exert anti-phage invasion effects,providing theoretical basis and new perspectives for the prevention and control of pathogenic bacteria and the development of efficient phage preparations.

关 键 词：NAD^(+) NAD^(+)水解酶 抗噬菌体 毒素 流产感染 

分 类 号：Q556[生物学—生物化学]