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Heat Shock Protein DnaJ in Pseudomonas aeruginosa Affects Biofilm Formation via Pyocyanin Production

机译:铜绿假单胞菌中的热激蛋白DnaJ通过生成花青素影响生物膜的形成。

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摘要

Heat shock proteins (HSPs) play important biological roles, and they are implicated in bacterial response to environmental stresses and in pathogenesis of infection. The role of HSPs in however, remains to be fully elucidated. Here, we report the unique role of HSP DnaJ in biofilm formation and pathogenicity in . A mutant produced hardly any pyocyanin and formed significantly less biofilms, which contributed to decreased pathogenicity as demonstrated by reduced mortality rate in a infection model. The reduced pyocyanin production in the mutant was a result of the decreased transcription of phenazine synthesis operons including , , , and . The reduction of biofilm formation and initial adhesion in the mutant could be reversed by exogenously added pyocyanin or extracellular DNA (eDNA). Consistent with such observations, absence of significantly reduced the release of eDNA in and addition of exogenous pyocyanin could restore eDNA release. These results indicate mutation caused reduced pyocyanin production, which in turn caused the decreased eDNA, resulting in decreased biofilm formation. DnaJ is required for pyocyanin production and full virulence in ; it affects biofilm formation and initial adhesion via pyocyanin, inducing eDNA release.
机译:热休克蛋白(HSP)发挥着重要的生物学作用,它们与细菌对环境压力的反应以及感染的发病机理有关。但是,HSP的作用尚待充分阐明。在这里,我们报告HSP DnaJ在生物膜形成和致病性中的独特作用。一个突变体几乎不产生任何一个卵黄蛋白,并且形成的生物膜明显减少,这有助于降低致病性,如感染模型中死亡率的降低所证明。突变体中减少的花青素产生是吩嗪合成操纵子包括,,和的转录减少的结果。生物膜形成的减少和突变体中初始黏附的减少可以通过外源添加黄绿素或细胞外DNA(eDNA)来逆转。与这些观察结果一致,不显着降低eDNA的释放以及添加外源性绿脓素可以恢复eDNA的释放。这些结果表明,突变引起的藻蓝蛋白产量减少,进而导致eDNA减少,从而导致生物膜形成减少。 DnaJ是产生花青素和充分毒力所需要的;它会通过藻蓝蛋白影响生物膜的形成和初始粘附,从而诱导eDNA释放。

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