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Indole inhibits bacterial quorum sensing signal transmission by interfering with quorum sensing regulator folding

机译:吲哚通过干扰群体感应调节剂折叠来抑制细菌群体感应信号传输

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Quorum sensing (QS)-dependent biofilm formation and motility were controlled by AqsR in Acinetobacter oleivorans DR1. QS-controlled phenotypes appeared to be inhibited by indole and the aqsR mutant had the same phenotypes. We demonstrated that the turnover rate of AqsR became more rapid without the N-acylhomoserine lactone (AHL) signal, and that indole could increase the expression of many protease and chaperone proteins. The addition of exogenous indole decreased the expression of two AqsR-targeted genes: AOLE_03905 (putative surface adhesion protein) and AOLE_11355 (l-asparaginase). The overexpression of AqsR in Escherichia coli was impossible with the indole treatment. Surprisingly, our [35S]methionine pulse-labelling data demonstrated that the stability and folding of AqsR protein decreased in the presence of indole without changing aqsR mRNA expression in E. coli. Interestingly, indole resulted in a loss of TraR-dependent traG expression in an Agrobacterium tumefaciens indicator strain. However, when indole was added after incubation with exogenous AHL, indole could not inhibit the TraR-dependent expression of the traG promoter. This indicated that AHL-bound TraR could be protective against indole, but TraR without AHL could not be active in the presence of indole. Here, we provided evidence for the first time showing that the indole effect on QS-controlled bacterial phenotypes is due to inhibited QS regulator folding and not a reduced QS signal.
机译:在油不动杆菌DR1中,AqsR控制了群体感应(QS)依赖性的生物膜形成和运动。 QS控制的表型似乎受到吲哚的抑制,而aqsR突变体具有相同的表型。我们证明没有N-酰基高丝氨酸内酯(AHL)信号,AqsR的周转率变得更快,并且吲哚可以增加许多蛋白酶和伴侣蛋白的表达。外源吲哚的添加降低了两个靶向AqsR的基因的表达:AOLE_03905(假定的表面粘附蛋白)和AOLE_11355(1-天冬酰胺酶)。用吲哚处理不可能在大肠杆菌中过表达AqsR。令人惊讶的是,我们的[35S]蛋氨酸脉冲标记数据表明,在吲哚存在下,AqsR蛋白的稳定性和折叠性降低了,而没有改变大肠杆菌中aqsR mRNA的表达。有趣的是,吲哚导致根癌农杆菌指示菌株中TraR依赖性traG表达的损失。但是,在与外源性AHL孵育后添加吲哚时,吲哚不能抑制traG启动子的TraR依赖性表达。这表明AHL结合的TraR可能对吲哚具有保护作用,但是没有AHL的TraR在存在吲哚的情况下不具有活性。在这里,我们首次提供证据表明,对QS控制的细菌表型的吲哚效应是由于抑制QS调节剂折叠而不是降低QS信号所致。

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