PDF(Pubmed)
Abstract：
Bacterial competition may rely on secretion systems such as the type 6 secretion system (T6SS), which punctures and releases toxic molecules into neighboring cells. To subsist, bacterial targets must counteract the threats posed by T6SS-positive competitors. In this study, we used a comprehensive genome-wide high-throughput screening approach to investigate the dynamics of interbacterial competition. Our primary goal was to identify deletion mutants within the well-characterized E. coli K-12 single-gene deletion library, the Keio collection, that demonstrated resistance to T6SS-mediated killing by the enteropathogenic bacterium Cronobacter malonaticus. We identified 49 potential mutants conferring resistance to T6SS and focused our interest on a deletion mutant (∆fimE) exhibiting enhanced expression of type 1 fimbriae. We demonstrated that the presence of type 1 fimbriae leads to the formation of microcolonies and thus protects against T6SS-mediated assaults. Collectively, our study demonstrated that adhesive structures such as type 1 fimbriae confer collective protective behavior against T6SS attacks.IMPORTANCEType 6 secretion systems (T6SS) are molecular weapons employed by gram-negative bacteria to eliminate neighboring microbes. T6SS plays a pivotal role as a virulence factor, enabling pathogenic gram-negative bacteria to compete with the established communities to colonize hosts and induce infections. Gaining a deeper understanding of bacterial interactions will allow the development of strategies to control the action of systems such as the T6SS that can manipulate bacterial communities. In this context, we demonstrate that bacteria targeted by T6SS attacks from the enteric pathogen Cronobacter malonaticus, which poses a significant threat to infants, can develop a collective protective mechanism centered on the production of type I fimbriae. These adhesive structures promote the aggregation of bacterial preys and the formation of microcolonies, which protect the cells from T6SS attacks.
摘要：
细菌竞争可能依赖于分泌系统，如6型分泌系统(T6SS)，刺破并释放有毒分子进入邻近细胞.为了生存，细菌靶标必须抵消T6SS阳性竞争者带来的威胁。在这项研究中,我们使用全面的全基因组高通量筛选方法来研究细菌间竞争的动态.我们的主要目标是在特征明确的大肠杆菌K-12单基因缺失文库中鉴定缺失突变体，Keio系列,证明了对肠道致病菌CronobacterMalonaticusT6SS介导的杀伤的抗性。我们鉴定了49个对T6SS具有抗性的潜在突变体，并将我们的兴趣集中在表现出1型菌毛表达增强的缺失突变体（ΔfimE）上。我们证明，1型菌毛的存在会导致微菌落的形成，从而防止T6SS介导的攻击。总的来说，我们的研究表明，粘合结构，如1型菌毛赋予集体保护行为，对T6SS攻击。IMPORTANCE6型分泌系统（T6SS）是革兰氏阴性菌用来消灭邻近微生物的分子武器。T6SS作为毒力因子起着举足轻重的作用，使致病性革兰氏阴性菌与已建立的群落竞争定植宿主并诱导感染。对细菌相互作用有更深入的了解将允许开发策略来控制系统的作用，例如可以操纵细菌群落的T6SS。在这种情况下，我们证明了T6SS攻击的目标细菌来自肠道病原体丙二酸梭菌，这对婴儿构成了重大威胁，可以发展以I型菌毛生产为中心的集体保护机制。这些粘附结构促进细菌猎物的聚集和微菌落的形成，保护细胞免受T6SS攻击。
