bifA Regulates Biofilm Development of Pseudomonas putida MnB1 as a Primary Response to H(2)O(2) and Mn(2).

bifA Regulates Biofilm Development of Pseudomonas putida MnB1 as a Primary Response to H(2)O(2) and Mn(2).
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DOI:
10.3389/fmicb.2018.01490
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发表时间:
2018
影响因子:
5.2
通讯作者:
Zhang D
Zhang D
中科院分区:
生物学2区
文献类型:
--
作者:
Zheng Y;Li Y;Long H;Zhao X;Jia K;Li J;Wang L;Wang R;Lu X;Zhang D

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恶臭假单胞菌MnB 1是环境科学与技术中广泛应用的微生物锰氧化的模式菌株。大量研究表明,恶臭假单胞菌MnB 1的生长和代谢受多种环境因子的影响。本文研究了过氧化氢(H2 O2)和锰(Mn 2+)对恶臭假单胞菌MnB 1增殖、Mn 2+获得、抗氧化系统和生物膜形成的影响。从恶臭假单胞菌GB 1中扩增了mco、mntABC、sod和bifA 4个相关基因的同源序列,并分别检测了它们的参与情况。我们发现恶臭假单胞菌MnB 1降解H2 O2,并迅速恢复增殖,但其细胞内的氧化应激状态得以维持,H2 O2耗尽后快速形成生物膜。通过qRT-PCR获得的mco、mntABC、sod和bifA表达水平的数据阐明了对bifA介导的生物膜形成的敏感性,与H2 O2暴露下的细胞内抗氧化系统相反。同时,Mn ~(2+)抑制了恶臭假单胞菌MnB 1的生物膜形成。这些基因的表达模式表明,锰离子供应可能起到调节生物膜形成的作用,而不仅仅是作为恶臭假单胞菌MnB 1的营养底物。此外,阻断BifA活性的GTP增加了生物膜的形成和发展过程中H2 O2暴露,而匡威反应Mn 2+离子供应是显而易见的。这些不同的细胞对H2 O2和Mn 2+的反应提供了对环境微生物免受外源因素影响的共同机制的见解。我们推测BifA介导的生物膜形成而非细胞内抗氧化系统可能是恶臭假单胞菌MnB 1采取的主要保护策略。这些发现将突出微生物适应机制的理解,以不同的环境压力。
Pseudomonas putida (P. putida) MnB1 is a widely used model strain in environment science and technology for determining microbial manganese oxidation. Numerous studies have demonstrated that the growth and metabolism of P. putida MnB1 are influenced by various environmental factors. In this study, we investigated the effects of hydrogen peroxide (H2O2) and manganese (Mn2+) on proliferation, Mn2+ acquisition, anti-oxidative system, and biofilm formation of P. putida MnB1. The related orthologs of 4 genes, mco, mntABC, sod, and bifA, were amplified from P. putida GB1 and their involvement were assayed, respectively. We found that P. putida MnB1 degraded H2O2, and quickly recovered for proliferation, but its intracellular oxidative stress state was maintained, with rapid biofilm formation after H2O2 depletion. The data from mco, mntABC, sod and bifA expression levels by qRT-PCR, elucidated a sensitivity toward bifA-mediated biofilm formation, in contrary to intracellular anti-oxidative system under H2O2 exposure. Meanwhile, Mn2+ ion supply inhibited biofilm formation of P. putida MnB1. The expression pattern of these genes showed that Mn2+ ion supply likely functioned to modulate biofilm formation rather than only acting as nutrient substrate for P. putida MnB1. Furthermore, blockade of BifA activity by GTP increased the formation and development of biofilms during H2O2 exposure, while converse response to Mn2+ ion supply was evident. These distinct cellular responses to H2O2 and Mn2+ provide insights on the common mechanism by which environmental microorganisms may be protected from exogenous factors. We postulate that BifA-mediated biofilm formation but not intracellular anti-oxidative system may be a primary protective strategy adopted by P. putida MnB1. These findings will highlight the understanding of microbial adaptation mechanisms to distinct environmental stresses.
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