Biofilms usually form when the density of bacteria increases during the middle to late periods of growth in culture, commonly induced by quorum-sensing systems. Biofilms attach to the surfaces of either living or nonliving objects and protect bacteria against antibiotics and a host’s immune system. Here, a novel type of biofilm (the “R-biofilm”) is reported. These biofilms were formed by clinically isolated Klebsiella pneumoniae strains following double-stranded-DNA breaks (DSBs), while undamaged bacteria did not form classic biofilms even in the later stages of growth. R-biofilms had a fixed ring-like or discoid shape with good ductility and could protect many living bacterial cells within. We show that extracellular proteins and DNAs released, probably by dead bacteria, were the core structural materials of R-biofilms. We anticipate that novel signaling pathways besides the bacterial SOS response are involved in R-biofilm formation. The observations in this study suggest a limitation to the use of the currently popular Cas9-mediated bactericidal tools to eliminate certain bacteria because the resulting DSBs may lead to the formation of these protective R-biofilms.

中文翻译：

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DNA断裂在肺炎克雷伯菌中诱导的非经典生物膜。

生物膜通常在细菌生长的中晚期达到细菌密度增加时形成，通常是由群体感应系统诱导的。生物膜附着在生物或非生物物体的表面，并保护细菌免受抗生素和宿主免疫系统的侵害。在此，报道了一种新型的生物膜（“ R-生物膜”）。这些生物膜是由临床分离的肺炎克雷伯菌形成的双链DNA断裂（DSB）之后的菌株，而即使在生长的后期，未受损的细菌也不会形成经典的生物膜。R-生物膜具有固定的环状或盘状形状，具有良好的延展性，可以保护其中的许多活细菌细胞。我们表明，可能由死亡细菌释放的细胞外蛋白质和DNA是R-生物膜的核心结构材料。我们预计，除了细菌SOS反应外，新型信号通路也参与了R-生物膜的形成。这项研究中的观察结果表明，限制使用目前流行的Cas9介导的杀菌工具消除某些细菌，因为所得的DSB可能导致这些保护性R-生物膜的形成。