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群体感应系统调控的耐热性的转录组分析 于……中 (原文句子不完整)

Transcriptome analysis of heat resistance regulated by quorum sensing system in .

作者信息

Zhang Bingzhou, Jiang Changsheng, Cao Hua, Zeng Wei, Ren Jingping, Hu Yaofang, Li Wentao, He Qigai

机构信息

State Key Laboratory of Agricultural Microbiology, College of Animal Sciences and Veterinary Medicine, Huazhong Agricultural University, Wuhan, China.

The Cooperative Innovation Center for Sustainable Pig Production, Huazhong Agricultural University, Wuhan, China.

出版信息

Front Microbiol. 2022 Aug 11;13:968460. doi: 10.3389/fmicb.2022.968460. eCollection 2022.

DOI:10.3389/fmicb.2022.968460
PMID:36033895
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9403865/
Abstract

The ability of bacteria to resist heat shock allows them to adapt to different environments. In addition, heat shock resistance is known for their virulence. Our previous study showed that the AI-2/luxS quorum sensing system affects the growth characteristics, biofilm formation, and virulence of . The resistance of quorum sensing system deficient to heat shock was obviously weaker than that of wild type strain. However, the regulatory mechanism of this phenotype remains unclear. To illustrate the regulatory mechanism by which the quorum sensing system provides resistance to heat shock, the transcriptomes of wild type (GPS2), ΔluxS, and complemented (C-luxS) strains were analyzed. Four hundred forty-four differentially expressed genes were identified in quorum sensing system deficient , which participated in multiple regulatory pathways. Furthermore, we found that regulates the expression of , , , , , and genes to resist heat shock the quorum sensing system. We further confirmed that and genes exerted an opposite regulatory effect on heat shock resistance. In conclusion, the findings of this study provide a novel insight into how the quorum sensing system affects the transcriptome of and regulates its heat shock resistance property.

摘要

细菌抵抗热休克的能力使它们能够适应不同的环境。此外,热休克抗性因其毒力而闻名。我们之前的研究表明,AI-2/luxS群体感应系统会影响[具体细菌名称]的生长特性、生物膜形成和毒力。群体感应系统缺陷型[具体细菌名称]对热休克的抗性明显弱于野生型菌株。然而,这种表型的调控机制仍不清楚。为了阐明群体感应系统赋予热休克抗性的调控机制,我们分析了野生型(GPS2)、ΔluxS和互补(C-luxS)菌株的转录组。在群体感应系统缺陷型[具体细菌名称]中鉴定出444个差异表达基因,它们参与了多种调控途径。此外,我们发现[具体细菌名称]通过群体感应系统调节[具体基因名称]、[具体基因名称]、[具体基因名称]、[具体基因名称]、[具体基因名称]和[具体基因名称]基因的表达以抵抗热休克。我们进一步证实,[具体基因名称]和[具体基因名称]基因对热休克抗性发挥相反的调控作用。总之,本研究结果为群体感应系统如何影响[具体细菌名称]的转录组并调节其热休克抗性特性提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/ff253268b020/fmicb-13-968460-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/ca9c3178478e/fmicb-13-968460-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/963feb2d32e4/fmicb-13-968460-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/e2011f23dedf/fmicb-13-968460-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/4868ca7a330a/fmicb-13-968460-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/4d65b4bcd8b7/fmicb-13-968460-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/ff253268b020/fmicb-13-968460-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/ca9c3178478e/fmicb-13-968460-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/963feb2d32e4/fmicb-13-968460-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/e2011f23dedf/fmicb-13-968460-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/4868ca7a330a/fmicb-13-968460-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/4d65b4bcd8b7/fmicb-13-968460-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac2/9403865/ff253268b020/fmicb-13-968460-g006.jpg

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