“化箭为'帆'”!南京农业大学教授,入选国家级人才,《Cell》旗下发表论文,提供生防细菌冲突化解方案

近日，南京农业大学植物保护学院钱国良教授团队在国际知名期刊Current Biology发表了题为“Effector-Mediated Transcriptional Rewiring Resolves Interbacterial Conflict Through Conserved c-di-GMP Antagonism”的研究论文。

该研究以生防细菌产酶溶杆菌（Lysobacter enzymogenes）与防御假单胞菌（Pseudomonas protegens）为模型，首次揭示了一种细菌解决种间冲突的全新范式——“防御-逃逸”（Defense-Escape）。研究发现，细菌不仅能防御竞争者的攻击，更能通过转录重编程，“劫持”敌方的效应蛋白作为信号分子，从而解除自身的运动抑制，实现战术突围。

AlphaFold3预测的LtaE与FleQ六聚体的复合物模型

这项研究虽然聚焦于微观分子的博弈，但其揭示的“防御-逃逸”模式，触及了生物防治和合成微生物组构建的核心难题，为该领域提供了全新的解决思路。

南京农业大学植保学院博士研究生徐富贵为论文第一作者，钱国良教授为论文的通讯作者，钟山青年研究员王冰鑫为论文的共同通讯作者。论文得到中国科学技术大学杨新星教授、南京农业大学窦道龙教授和艾干博士、浙江大学王蒙岑教授、兰州大学何永兴教授、蒙大拿州立大学闫庆教授的大力帮助。

Summary

Microbial competition serves as a fundamental driver for the evolution of offensive and defensive mechanisms among microorganisms. While it is well established that bacteria utilize specialized secretion systems to deliver both toxic and non-toxic effector proteins into competing cells, thereby directly killing them or modulating cellular events, it remains largely unclear whether bacteria can hijack effector proteins derived from competitors to resolve interspecies conflicts. Here, we demonstrate that Pseudomonas protegens employs a sophisticated defense strategy, hijacking LtaE, a non-cytotoxic effector delivered via the type IV secretion system (T4SS) of non-flagellated Lysobacter enzymogenes, to resolve interbacterial conflict through transcriptional reprogramming. Translocated LtaE neutralizes an uncharacterized antibacterial toxin in P. protegens. Surprisingly, as a countermeasure, P. protegens hijacks LtaE to rewire its host signaling hierarchy, converting it into a motility activation switch. Mechanistically, LtaE directly binds to FleQ, the σ54-dependent master regulator of flagellar biosynthesis, shielding it from inhibitory c-di-guanosine monophosphate (GMP) binding—a universal second messenger whose elevated concentration typically inhibits bacterial motility and promotes biofilm formation. Remarkably, the LtaE-FleQ complex remains stable under high c-di-GMP conditions, overriding sessility signals to derepress flagellar gene expression and trigger escape motility. Biochemical analyses reveal that LtaE broadly targets FleQ homologs across pseudomonads through competitive inhibition of c-di-GMP binding, linking competitor detection to motility activation. Our findings establish a novel bacterial conflict-resolution paradigm, demonstrating how non-cytotoxic effectors act as molecular switches to dynamically reprogram transcriptional networks and enhance phenotypic plasticity.

原文链接：https://www.cell.com/current-biology/fulltext/S0960-9822(25)01612-4