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由必需的YycFG双组分系统控制的基因的鉴定揭示了生物膜调节在……中的作用 。 (原文最后似乎不完整)

Identification of Genes Controlled by the Essential YycFG Two-Component System Reveals a Role for Biofilm Modulation in .

作者信息

Xu Tao, Wu Yang, Lin Zhiwei, Bertram Ralph, Götz Friedrich, Zhang Ying, Qu Di

机构信息

Key Laboratory of Medical Molecular Virology of Ministries of Education and Health, Department of Medical Microbiology and Parasitology, Institute of Medical Microbiology and Institutes of Biomedical Sciences, Fudan UniversityShanghai, China.

Key Laboratory of Medical Molecular Virology, Huashan Hospital, Shanghai Medical College of Fudan UniversityShanghai, China.

出版信息

Front Microbiol. 2017 Apr 26;8:724. doi: 10.3389/fmicb.2017.00724. eCollection 2017.

Abstract

Biofilms play a crucial role in the pathogenicity of , while little is known about whether the essential YycFG two-component signal transduction system (TCS) is involved in biofilm formation. We used antisense RNA (asRNA) to silence the TCS in order to study its regulatory functions in . Strain 1457 expressing asRNA exhibited a significant delay (~4-5 h) in entry to log phase, which was partially complemented by overexpressing . The expression of asRNA and asRNA resulted in a 68 and 50% decrease in biofilm formation at 6 h, respectively, while they had no significant inhibitory effect on 12 h biofilm formation. The expression of asRNA led to a ~5-fold increase in polysaccharide intercellular adhesion (PIA) production, but it did not affect the expression of accumulation-associated protein (Aap) or the release of extracellular DNA. Consistently, quantitative real-time PCR showed that silencing resulted in an increased transcription of biofilm-related genes, including , and . An search of the YycF regulon for the conserved YycF recognition pattern and a modified motif in , along with additional gel shift and DNase I footprinting assays, showed that , and are directly regulated by YycF. Our data suggests that YycFG modulates biofilm formation in an ica-dependent manner.

摘要

生物膜在[具体病原体名称未给出]的致病性中起关键作用,而关于必需的YycFG双组分信号转导系统(TCS)是否参与生物膜形成知之甚少。我们使用反义RNA(asRNA)使TCS沉默,以研究其在[具体病原体名称未给出]中的调控功能。表达asRNA的菌株1457进入对数期出现显著延迟(约4 - 5小时),过表达[相关基因未给出]可部分弥补这一延迟。asRNA[具体编号未给出]和asRNA[具体编号未给出]的表达分别导致6小时时生物膜形成减少68%和50%,而对12小时生物膜形成无显著抑制作用。asRNA[具体编号未给出]的表达导致细胞间多糖黏附(PIA)产量增加约5倍,但不影响积累相关蛋白(Aap)的表达或细胞外DNA的释放。同样,定量实时PCR表明沉默[相关基因未给出]导致生物膜相关基因转录增加,包括[具体基因未给出]、[具体基因未给出]和[具体基因未给出]。对YycF调控子进行搜索,寻找保守的YycF识别模式以及[具体基因未给出]中的修饰基序,同时进行额外的凝胶迁移和DNase I足迹分析,结果表明[具体基因未给出]、[具体基因未给出]和[具体基因未给出]受YycF直接调控。我们的数据表明,YycFG以ica依赖的方式调节[具体病原体名称未给出]生物膜的形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adc1/5405149/8d8603d10f16/fmicb-08-00724-g0001.jpg

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