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TatD脱氧核糖核酸酶有助于生物膜形成和在……中的毒力。 (原文不完整,此为根据现有内容的翻译)

TatD DNases Contribute to Biofilm Formation and Virulence in .

作者信息

Zhang Zehui, Liang Yinfeng, Yu Lihui, Chen Menghan, Guo Yuru, Kang Zhiruo, Qu Chenghu, Tian Chunlian, Zhang Dexian, Liu Mingchun

机构信息

Key Laboratory of Livestock Infectious Diseases in Northeast China, Ministry of Education, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang, China.

出版信息

Front Microbiol. 2021 Nov 15;12:758465. doi: 10.3389/fmicb.2021.758465. eCollection 2021.

DOI:10.3389/fmicb.2021.758465
PMID:34867886
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8634637/
Abstract

TatD DNases are conserved proteins in a variety of organisms and are considered potential virulence factors in and . However, the function of TatD DNases has not yet been determined in , which causes various infections in animals and leads to economic losses. In this study, we describe the roles of TatD DNases in (TpTatDs). A bioinformatics analysis was performed to investigate the sequence characteristics of TpTatDs, and then the ability of recombinant TatD proteins to hydrolyze DNA was determined in the presence of divalent cations. Moreover, we constructed -deficient mutants. The biofilms formed by the wild-type and mutant strains were observed under a microscope. The mortality and bacterial load in the spleen of mice infected with the wild-type strain and -deficient mutants were determined to obtain insights into the role of TatDs in the virulence of Two TatD DNases were identified in . They were Mg-dependent DNases and exhibited DNA endonuclease activity. Compared with those formed by the parental strain, biofilms formed by mutants showed a significantly reduced thickness and biomass. Moreover, mutants produced a lower bacterial load in the spleen of mice and compromised virulence. Our data indicated that TatD DNases in are involved in biofilm formation and required for virulence during infections.

摘要

TatD脱氧核糖核酸酶是多种生物体中保守的蛋白质,被认为是[具体两种生物]中的潜在毒力因子。然而,TatD脱氧核糖核酸酶在[某种生物]中的功能尚未确定,该生物会导致动物的各种感染并造成经济损失。在本研究中,我们描述了TatD脱氧核糖核酸酶在[该生物名称缩写为TpTatDs]中的作用。进行了生物信息学分析以研究TpTatDs的序列特征,然后在二价阳离子存在的情况下测定重组TatD蛋白水解DNA的能力。此外,我们构建了[具体基因]缺陷型突变体。在显微镜下观察野生型和突变株形成的生物膜。测定感染野生型菌株和[具体基因]缺陷型突变体的小鼠脾脏中的死亡率和细菌载量,以深入了解TatDs在[该生物名称]毒力中的作用。在[该生物名称]中鉴定出两种TatD脱氧核糖核酸酶。它们是镁依赖性脱氧核糖核酸酶,并表现出DNA内切酶活性。与亲本菌株形成的生物膜相比,突变体形成的生物膜厚度和生物量显著降低。此外,突变体在小鼠脾脏中产生的细菌载量较低且毒力受损。我们的数据表明,[该生物名称]中的TatD脱氧核糖核酸酶参与生物膜形成,并且在感染期间的毒力中是必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/6b804cf0e8ff/fmicb-12-758465-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/6f70cdc20385/fmicb-12-758465-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/abdefacae619/fmicb-12-758465-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/72f5143581f5/fmicb-12-758465-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/9ec4a6ea97a1/fmicb-12-758465-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/7901311b01af/fmicb-12-758465-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/00d5000e564e/fmicb-12-758465-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/6b804cf0e8ff/fmicb-12-758465-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/6f70cdc20385/fmicb-12-758465-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/abdefacae619/fmicb-12-758465-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/72f5143581f5/fmicb-12-758465-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/9ec4a6ea97a1/fmicb-12-758465-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/7901311b01af/fmicb-12-758465-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/00d5000e564e/fmicb-12-758465-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/618b/8634637/6b804cf0e8ff/fmicb-12-758465-g007.jpg

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