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群集细菌经历局部动态相变,形成应激诱导生物膜。

Swarming bacteria undergo localized dynamic phase transition to form stress-induced biofilms.

机构信息

Warwick Medical School, Universityof Warwick, Coventry, United Kingdom.

Centre for Mechanochemical Cell Biology, University of Warwick, Coventry, United Kingdom.

出版信息

Elife. 2021 Mar 16;10:e62632. doi: 10.7554/eLife.62632.

Abstract

Self-organized multicellular behaviors enable cells to adapt and tolerate stressors to a greater degree than isolated cells. However, whether and how cellular communities alter their collective behaviors adaptively upon exposure to stress is largely unclear. Here, we investigate this question using , a model system for bacterial multicellularity. We discover that, upon exposure to a spatial gradient of kanamycin, swarming bacteria activate matrix genes and transit to biofilms. The initial stage of this transition is underpinned by a stress-induced multilayer formation, emerging from a biophysical mechanism reminiscent of motility-induced phase separation (MIPS). The physical nature of the process suggests that stressors which suppress the expansion of swarms would induce biofilm formation. Indeed, a simple physical barrier also induces a swarm-to-biofilm transition. Based on the gained insight, we propose a strategy of antibiotic treatment to inhibit the transition from swarms to biofilms by targeting the localized phase transition.

摘要

自组织的多细胞行为使细胞能够比孤立的细胞更好地适应和耐受应激源。然而,细胞群体在暴露于应激时是否以及如何适应性地改变其集体行为在很大程度上尚不清楚。在这里,我们使用 ,一种细菌多细胞性的模型系统,来研究这个问题。我们发现,当暴露于卡那霉素的空间梯度时,群集细菌会激活基质基因并过渡到生物膜。这种转变的初始阶段是由一种应激诱导的多层形成支撑的,这种形成源于一种类似于运动诱导相分离(MIPS)的生物物理机制。该过程的物理性质表明,抑制群集扩展的应激源会诱导生物膜的形成。事实上,一个简单的物理障碍也会诱导从群集到生物膜的转变。基于所获得的见解,我们提出了一种抗生素治疗策略,通过靶向局部相变来抑制从群集到生物膜的转变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3f1/7963483/a90f14f0f35c/elife-62632-fig1.jpg

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