Flagellar Perturbations Activate Adhesion through Two Distinct Pathways in Caulobacter crescentus.
Flagellar Perturbations Activate Adhesion through Two Distinct Pathways in Caulobacter crescentus.
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DOI：
10.1128/mbio.03266-20
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发表时间：
2021-02-09
期刊：
影响因子：
6.4
通讯作者：
Crosson S
中科院分区：
文献类型：
--
作者：
Hershey DM;Fiebig A;Crosson S
了解细菌如何在固体表面定植具有重要的临床、工业和生态意义。在这项研究中，我们确定了新月柄杆菌激活表面附着所需的基因，以响应来自称为鞭毛的大分子机器的信号。细菌执行复杂的发育程序来定殖外源表面。旋转鞭毛是驱动运动的动力机器，是表面殖民的关键调节器。鞭毛识别的特定信号和这些信号被转导以协调粘附的途径仍然是争论的主题。突变破坏了二型细菌新月柄杆菌中鞭毛的组装，刺激了一种称为固着物的多糖粘附素的产生。使用全基因组表型分析方法，我们比较了野生型和鞭毛突变背景下的C。crescentus。我们发现了一组不同的鞭毛突变，通过诱导hyperholdfast表型来增强粘附，并发现了第二组抑制这种表型的突变。对鞭毛信号抑制子（fss）突变的上位性分析表明，鞭毛通过两条遗传上不同的途径刺激固着物的产生。发育调节PleD有助于在鞭毛组装的早期和晚期阶段破坏突变体的固着诱导。突变体破坏后期阶段的鞭毛组装，组装一个完整的转子复合物，诱导holdfast生产通过一个额外的过程，需要的MotAB定子及其相关的二鸟苷酸环化酶，DgcB。我们已经将fss基因的一个子集分配给定子依赖性网络或pleD依赖性网络，并表征了两个先前未识别的运动基因，它们通过定子复合体调节固着物的产生。我们提出了一个模型，通过鞭毛整合机械刺激到C。crescentus的发展计划，以协调粘附。
Understanding how bacteria colonize solid surfaces is of significant clinical, industrial and ecological importance. In this study, we identified genes that are required for Caulobacter crescentus to activate surface attachment in response to signals from a macromolecular machine called the flagellum. Bacteria carry out sophisticated developmental programs to colonize exogenous surfaces. The rotary flagellum, a dynamic machine that drives motility, is a key regulator of surface colonization. The specific signals recognized by flagella and the pathways by which those signals are transduced to coordinate adhesion remain subjects of debate. Mutations that disrupt flagellar assembly in the dimorphic bacterium Caulobacter crescentus stimulate the production of a polysaccharide adhesin called the holdfast. Using a genomewide phenotyping approach, we compared surface adhesion profiles in wild-type and flagellar mutant backgrounds of C. crescentus. We identified a diverse set of flagellar mutations that enhance adhesion by inducing a hyperholdfast phenotype and discovered a second set of mutations that suppress this phenotype. Epistasis analysis of the flagellar signaling suppressor (fss) mutations demonstrated that the flagellum stimulates holdfast production via two genetically distinct pathways. The developmental regulator PleD contributes to holdfast induction in mutants disrupted at both early and late stages of flagellar assembly. Mutants disrupted at late stages of flagellar assembly, which assemble an intact rotor complex, induce holdfast production through an additional process that requires the MotAB stator and its associated diguanylate cyclase, DgcB. We have assigned a subset of the fss genes to either the stator- or pleD-dependent networks and characterized two previously unidentified motility genes that regulate holdfast production via the stator complex. We propose a model through which the flagellum integrates mechanical stimuli into the C. crescentus developmental program to coordinate adhesion.