Zeng Bo, Wang Chong, Zhang Pansong, Guo Zisheng, Chen Lin, Duan Kangmin
Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Northwest University, Xi'an, Shaanxi 710069, China.
Department of Oral Biology & Medical Microbiology & Infectious Diseases, Rady Faculty of Health Sciences, University of Manitoba, 780 Bannatyne Ave., Winnipeg, MB R3E 0W2, Canada.
Microorganisms. 2020 Mar 12;8(3):395. doi: 10.3390/microorganisms8030395.
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.
热休克蛋白(HSPs)发挥着重要的生物学作用,它们与细菌对环境应激的反应以及感染的发病机制有关。然而,HSPs在[具体细菌名称未给出]中的作用仍有待充分阐明。在此,我们报告了HSP DnaJ在[具体细菌名称未给出]生物膜形成和致病性中的独特作用。一个[具体细菌名称未给出]的突变体几乎不产生绿脓菌素,形成的生物膜也明显较少,这导致其致病性降低,如在[具体细菌名称未给出]感染模型中死亡率降低所示。[具体细菌名称未给出]突变体中绿脓菌素产量的降低是包括[具体基因名称未给出]、[具体基因名称未给出]、[具体基因名称未给出]和[具体基因名称未给出]在内的吩嗪合成操纵子转录减少的结果。[具体细菌名称未给出]突变体中生物膜形成和初始黏附的减少可通过外源添加绿脓菌素或细胞外DNA(eDNA)来逆转。与这些观察结果一致,[具体细菌名称未给出]的缺失显著降低了[具体细菌名称未给出]中eDNA的释放,而添加外源绿脓菌素可恢复eDNA的释放。这些结果表明,[具体细菌名称未给出]突变导致绿脓菌素产量降低,进而导致eDNA减少,从而导致生物膜形成减少。DnaJ是[具体细菌名称未给出]产生绿脓菌素和完全毒力所必需的;它通过绿脓菌素影响生物膜形成和初始黏附,诱导eDNA释放。