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SPD_0090对……的毒力有负面影响。 （原句不完整，翻译可能不太准确，需结合完整原文进一步完善）

SPD_0090 Negatively Contributes to Virulence of .

作者信息

Cao Linlin, Li Nan, Dong Yingshan, Yang Xiao-Yan, Liu Jiajia, He Qing-Yu, Ge Ruiguang, Sun Xuesong

机构信息

MOE Key Laboratory of Tumor Molecular Biology and Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes, Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou, China.

State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.

出版信息

Front Microbiol. 2022 Jun 13;13:896896. doi: 10.3389/fmicb.2022.896896. eCollection 2022.

DOI:10.3389/fmicb.2022.896896
PMID:35770170
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9234739/
Abstract

In most bacteria, iron plays an important role in the survival of bacteria and the process of infection to the host. () evolved three iron transporters (i.e., PiaABC, PiuABC, and PitABC) responsible for the transportation of three kinds of iron (i.e., ferrichrome, hemin, and ferric ion). Our previous study showed that both mRNA and protein levels of SPD_0090 were significantly upregulated in the ΔΔΔ triple mutant, but its detailed biological function is unknown. In this study, we constructed _ knockout and complement strain and found that the deletion of hinders bacterial growth. SPD_0090 is located on the cell membrane and affects the hemin utilization ability of . The cell infection model showed that the knockout strain had stronger invasion and adhesion ability. Notably, knockout of the _ gene resulted in an enhanced infection ability of in mice by increasing the expression of virulence factors. Furthermore, iTRAQ quantitative proteomics studies showed that the knockout of inhibited carbon metabolism and thus suppressed bacterial growth. Our study showed that SPD_0090 negatively regulates the virulence of

摘要

在大多数细菌中，铁在细菌的生存以及对宿主的感染过程中发挥着重要作用。（某细菌）进化出了三种铁转运蛋白（即PiaABC、PiuABC和PitABC），分别负责转运三种铁（即铁载体、血红素和铁离子）。我们之前的研究表明，在ΔΔΔ三重突变体中，SPD_0090的mRNA和蛋白质水平均显著上调，但其具体生物学功能尚不清楚。在本研究中，我们构建了（该基因）敲除菌株和互补菌株，发现敲除（该基因）会阻碍细菌生长。SPD_0090位于细胞膜上，影响（该细菌）对血红素的利用能力。细胞感染模型显示，敲除菌株具有更强的侵袭和黏附能力。值得注意的是，敲除（该）基因通过增加毒力因子的表达，增强了（该细菌）在小鼠体内的感染能力。此外，iTRAQ定量蛋白质组学研究表明，敲除（该基因）会抑制碳代谢，从而抑制细菌生长。我们的研究表明，SPD_0090对（该细菌）的毒力起负调控作用

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/51acd971d91d/fmicb-13-896896-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/539acfddef39/fmicb-13-896896-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/0bb9271a70c4/fmicb-13-896896-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/9b284a72822c/fmicb-13-896896-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/a71b4f2a9443/fmicb-13-896896-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/a356a20838ad/fmicb-13-896896-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/e37d0297552a/fmicb-13-896896-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/5a5a92ea1515/fmicb-13-896896-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/51acd971d91d/fmicb-13-896896-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/539acfddef39/fmicb-13-896896-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/0bb9271a70c4/fmicb-13-896896-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/9b284a72822c/fmicb-13-896896-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/a71b4f2a9443/fmicb-13-896896-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/a356a20838ad/fmicb-13-896896-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/e37d0297552a/fmicb-13-896896-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/5a5a92ea1515/fmicb-13-896896-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6229/9234739/51acd971d91d/fmicb-13-896896-g008.jpg

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