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FliY和YdjN参与半胱氨酸/胱氨酸利用、抗氧化性及生物膜形成,但不是毒力的决定因素。

FliY and YdjN are involved in cysteine/cystine utilization, oxidative resistance, and biofilm formation but are not determinants of virulence.

作者信息

Zhao Fan, Xu Huan, Chen Yubing, Xiao Juan, Zhang Miao, Li Zhuo, Liu Jinlin, Qi Chao

机构信息

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, Hubei, China.

出版信息

Front Microbiol. 2023 May 12;14:1169774. doi: 10.3389/fmicb.2023.1169774. eCollection 2023.

DOI:10.3389/fmicb.2023.1169774
PMID:37250053
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10213525/
Abstract

INTRODUCTION

() is a member of in family Pasteurellaceae. It is the causative agent of porcine pleuropneumonia, which has caused huge economic losses to pig industry over the world. Cysteine is a precursor of many important biomolecules and defense compounds in the cell. However, molecular mechanisms of cysteine transport in are unclear.

METHODS

In this study, gene-deleted mutants were generated and investigated, to reveal the roles of potential cysteine/cystine transport proteins FliY and YdjN of .

RESULTS

Our results indicated that the growth of was not affected after or single gene deletion, but absence of both FliY and YdjN decreased the growth ability significantly, when cultured in the chemically defined medium (CDM) supplemented with cysteine or cystine as the only sulfur source. double deletion mutant ΔΔ showed increased sensitivity to oxidative stress. Besides, -complementation of YdjN into ΔΔ and wild type leads to increased biofilm formation in CDM. However, the virulence of ΔΔ was not attenuated in mice or pigs.

DISCUSSION

These findings suggest that FliY and YdjN are involved in the cysteine/cystine acquisition, oxidative tolerance, and biofilm formation, but not contribute to the pathogenicity of .

摘要

引言

()是巴斯德氏菌科的成员。它是猪胸膜肺炎的病原体,给全球养猪业造成了巨大经济损失。半胱氨酸是细胞中许多重要生物分子和防御化合物的前体。然而,()中半胱氨酸转运的分子机制尚不清楚。

方法

在本研究中,构建并研究了基因缺失突变体,以揭示()潜在的半胱氨酸/胱氨酸转运蛋白FliY和YdjN的作用。

结果

我们的结果表明,在以半胱氨酸或胱氨酸作为唯一硫源的化学限定培养基(CDM)中培养时,单基因缺失或后,()的生长不受影响,但FliY和YdjN均缺失会显著降低其生长能力。双缺失突变体ΔΔ对氧化应激的敏感性增加。此外,将YdjN互补到ΔΔ和野生型中会导致CDM中生物膜形成增加。然而,ΔΔ在小鼠或猪中的毒力并未减弱。

讨论

这些发现表明,()的FliY和YdjN参与半胱氨酸/胱氨酸的获取、氧化耐受性和生物膜形成,但对()的致病性没有贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/95b9efb99065/fmicb-14-1169774-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/c8b054d2f901/fmicb-14-1169774-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/d08475f14092/fmicb-14-1169774-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/ebfa0d997ad5/fmicb-14-1169774-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/d4b250df4b3e/fmicb-14-1169774-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/fdca2de4ec47/fmicb-14-1169774-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/95b9efb99065/fmicb-14-1169774-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/c8b054d2f901/fmicb-14-1169774-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/d08475f14092/fmicb-14-1169774-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/ebfa0d997ad5/fmicb-14-1169774-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/d4b250df4b3e/fmicb-14-1169774-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/fdca2de4ec47/fmicb-14-1169774-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea78/10213525/95b9efb99065/fmicb-14-1169774-g0006.jpg

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