Discovery of Calcium as a Biofilm-Promoting Signal for Vibrio fischeri Reveals New Phenotypes and Underlying Regulatory Complexity
Discovery of Calcium as a Biofilm-Promoting Signal for Vibrio fischeri Reveals New Phenotypes and Underlying Regulatory Complexity
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DOI：
10.1128/jb.00016-18
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发表时间：
2018-08-01
影响因子：
3.2
通讯作者：
Visick, Karen L.
中科院分区：
文献类型：
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作者：
Tischler, Alice H.;Lie, Louise;Visick, Karen L.
费氏弧菌利用生物膜的形成促进其乌贼宿主的共生定植。生物膜的形成是由一组复杂的双组分调控因子在共生多糖（syp）位点的转录水平上施加的。生物膜的形成可以通过传感器激酶RscS的过量产生来诱导，这需要杂交传感器激酶SypF和反应调节因子SypG的活性，并由传感器激酶BinK负调控。在这里，我们发现钙是一种信号，可以促进生物膜胜任菌株在生物膜通常不被观察到的条件下形成生物膜（晃动生长）。对于rscs过量产生的细胞以及仅删除负调节因子binK的菌株都是如此。后者的结果首次提供了在没有调节因子过表达的情况下诱导和评估生物膜形成的机会。在这些条件下，我们确定钙在这些位点的转录水平上诱导syp依赖性和细菌纤维素合成（bcs）依赖性生物膜。钙诱导的生物膜依赖于SypF，但SypF的Hpt结构域足以形成生物膜。这些数据表明另一种传感器激酶(s)的参与，并导致发现RscS和以前未被表征的传感器激酶HahK都在这一途径中起作用。总之，这里提出的数据揭示了fischeri细胞产生的新的信号和生物膜表型，参与不同生物膜行为的两种多糖的协调生产，以及有助于控制这些过程的新调节剂。生物膜，或通过通常包括多糖的基质附着的表面附着微生物群落，对环境胁迫具有高度抗性，因此在临床中存在问题，并且具有重要的研究意义。费氏弧菌形成生物膜来定植其共生宿主，使这种生物对研究生物膜很有用。生物膜的形成取决于多糖位点及其调控因子。在这里，我们确定了一个信号，钙，诱导SYP-PS和纤维素依赖的生物膜。我们还发现了一个新的syp调节因子，即传感器激酶HahK，并发现了传感器激酶RscS的突变表型。因此，这项工作揭示了一个协调控制两种多糖的特定生物膜诱导信号，鉴定了一个新的调节因子，并阐明了费氏弧菌对生物膜形成的调节控制。
Vibrio fischeri uses biofilm formation to promote symbiotic colonization of its squid host, Euprymna scolopes. Control over biofilm formation is exerted at the level of transcription of the symbiosis polysaccharide (syp) locus by a complex set of two-component regulators. Biofilm formation can be induced by overproduction of the sensor kinase RscS, which requires the activities of the hybrid sensor kinase SypF and the response regulator SypG and is negatively regulated by the sensor kinase BinK. Here, we identify calcium as a signal that promotes biofilm formation by biofilm-competent strains under conditions in which biofilms are not typically observed (growth with shaking). This was true for RscS-overproducing cells as well as for strains in which only the negative regulator binK was deleted. The latter results provided, for the first time, an opportunity to induce and evaluate biofilm formation without regulator overexpression. Using these conditions, we determined that calcium induces both syp-dependent and bacterial cellulose synthesis (bcs)-dependent biofilms at the level of transcription of these loci. The calcium-induced biofilms were dependent on SypF, but SypF's Hpt domain was sufficient for biofilm formation. These data suggested the involvement of another sensor kinase(s) and led to the discovery that both RscS and a previously uncharacterized sensor kinase, HahK, functioned in this pathway. Together, the data presented here reveal both a new signal and biofilm phenotype produced by V. fischeri cells, the coordinate production of two polysaccharides involved in distinct biofilm behaviors, and a new regulator that contributes to control over these processes.IMPORTANCE Biofilms, or communities of surface-attached microorganisms adherent via a matrix that typically includes polysaccharides, are highly resistant to environmental stresses and are thus problematic in the clinic and important to study. Vibrio fischeri forms biofilms to colonize its symbiotic host, making this organism useful for studying biofilms. Biofilm formation depends on the syp polysaccharide locus and its regulators. Here, we identify a signal, calcium, that induces both SYP-PS and cellulose-dependent biofilms. We also identify a new syp regulator, the sensor kinase HahK, and discover a mutant phenotype for the sensor kinase RscS. This work thus reveals a specific biofilm-inducing signal that coordinately controls two polysaccharides, identifies a new regulator, and clarifies the regulatory control over biofilm formation by V. fischeri.