Escherichia coli heat-shock proteins IbpA and Ibpb affect biofilm formation by influencing the level of extracellular indole
Escherichia coli heat-shock proteins IbpA and Ibpb affect biofilm formation by influencing the level of extracellular indole
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DOI：
10.1099/mic.0.032334-0
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发表时间：
2010-01-01
期刊：
影响因子：
2.8
通讯作者：
Laskowska, Ewa
中科院分区：
文献类型：
--
作者：
Kuczynska-Wisnik, Dorota;Matuszewska, Ewelina;Laskowska, Ewa
大肠杆菌生物膜的发展需要涉及细胞信号传导、应激反应、运动性和负责细胞附着的结构的合成的各种基因的差异表达。ibpAB操纵子是大肠杆菌生长期间最常诱导的应激反应基因之一。大肠杆菌生物膜。在这项研究中，我们证明，据我们所知，第一次，缺乏IbpAB蛋白在E。大肠杆菌细胞抑制在空气-液体界面处bofilm的形成，尽管它允许正常的增殖性生长。我们发现，ibpAB突变体细胞经历内源性氧化应激，这可能是由于过氧化氢酶活性下降。在ibpAB细胞中的内源性氧化应激导致增加的表达的异硫氰酸酯酶，一种催化吲哚合成的酶。我们证明了由ibpAB突变体形成的生物膜由于吲哚的细胞外浓度的增加而延迟，吲哚已知发挥信号分子的作用，抑制生物膜生长。
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 bofilm 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.