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Escherichia coli heat-shock proteins IbpA and IbpB affect biofilm formation by influencing the level of extracellular indole

机译:大肠杆菌热冲击蛋白IBPA和IBPB通过影响细胞外吲哚的水平影响生物膜形成

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The development of Escherichia coli biofilm requires the differential expression of various genes implicated in cell signalling, stress responses, motility and the synthesis of structures responsible for cell attachment. The ibpAB operon is among the stress-response genes most induced during growth of the E. coli biofilm. In this study we demonstrated, to our knowledge for the first time, that the lack of IbpAB proteins in E. coli cells inhibited the formation of biofilm at the air–liquid interface, although it allowed normal planktonic growth. We showed that ibpAB mutant cells experienced endogenous oxidative stress, which might result from a decreased catalase activity. The endogenous oxidative stress in ibpAB cells led to increased expression of tryptophanase, an enzyme which catalyses the synthesis of indole. We demonstrated that the formation of biofilm by the ibpAB mutant was delayed due to the increase in the extracellular concentration of indole, which is known to play the role of a signal molecule, inhibiting biofilm growth.
机译:大肠杆菌生物膜的发展需要涉及细胞信号传导,应力响应,运动和合成的各种基因的差异表达,该结构负责细胞附着物。 IBPAB操纵子是在大肠杆菌生物膜生长期间诱导的应激反应基因。在这项研究中,我们首次证明了我们的知识,即大肠杆菌细胞中缺乏IBPAB蛋白抑制在空气液体界面处形成生物膜的形成,尽管它允许正常的浮游生生长。我们表明IBPAB突变体细胞经历了内源性氧化应激,这可能由降低的过氧化氢酶活性导致。 IBPAB细胞内源性氧化应激导致色氨酸酶的表达增加,该酶催化吲哚合成的酶。我们证明,由于吲哚的细胞外浓度的增加,延迟了Ibpab突变体的生物膜的形成,这是已知发挥信号分子的作用,抑制生物膜生长的作用。

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