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壁磷壁酸上缺乏N-乙酰葡糖胺糖基化通过与细菌表面排斥来促进脂肪酸耐受性。

Absence of N-Acetylglucosamine Glycosylation on Wall Teichoic Acids Promotes Fatty Acid Tolerance by Repulsion From the Bacterial Surface.

作者信息

Thomasen Rikke S S, Dos Santos Patricia T, Sternkopf Lillebæk Eva M, Skov Marianne N, Kemp Michael, Kallipolitis Birgitte H

机构信息

Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark.

National Food Institute, Technical University of Denmark, Kgs. Lyngby, Denmark.

出版信息

Front Microbiol. 2022 May 12;13:897682. doi: 10.3389/fmicb.2022.897682. eCollection 2022.

Abstract

Free fatty acids (FFAs) have strong antimicrobial properties against pathogenic bacteria and are known as natural protective agents against bacterial infections. Growth of the foodborne pathogen is highly affected by the presence of antimicrobial FFAs, however, the response of toward FFAs is not fully understood. Here, we explore how gains tolerance toward FFAs and present a novel mechanism conferring bacterial protection against FFA toxicity. Strains tolerant against the antimicrobial FFA palmitoleic acid were isolated and whole genome sequenced, and mutations were found in genes involved in wall teichoic acid (WTA) glycosylations. We show that mutation or deletion of , which is essential for N-acetylglucosamine (GlcNAc) glycosylation of WTAs, confer tolerance against several antimicrobial FFAs. The FFA tolerant strains are lacking GlcNAc on their WTAs, which result in a more hydrophilic surface. In line with this, we observed a reduced binding of FFAs to the surface of the FFA tolerant strains. Additionally, lack of GlcNAc on WTAs confers tolerance toward acid stress. Altogether, these findings support that GlcNAc modification of WTA plays an important role in the response of toward stress conditions encountered during growth as a saprophyte and pathogen, including FFA-rich environments. Most importantly, our data revealed that strains lacking GlcNAc on their WTAs are protected against FFA toxicity, because the FFAs are repulsed from the bacterial surface of GlcNAc-deficient strains.

摘要

游离脂肪酸(FFAs)对病原菌具有强大的抗菌特性,被认为是抵抗细菌感染的天然保护剂。食源性病原体的生长受到抗菌FFAs存在的高度影响,然而,其对FFAs的反应尚未完全了解。在此,我们探究了[具体病原体名称未给出]如何获得对FFAs的耐受性,并提出了一种赋予细菌抵御FFA毒性的新机制。分离出对抗菌FFA棕榈油酸具有耐受性的菌株并进行全基因组测序,发现在参与壁磷壁酸(WTA)糖基化的基因中存在突变。我们表明,WTA的N - 乙酰葡糖胺(GlcNAc)糖基化所必需的[具体基因名称未给出]的突变或缺失赋予了对几种抗菌FFAs的耐受性。FFA耐受菌株的WTA上缺乏GlcNAc,这导致其表面更具亲水性。与此一致,我们观察到FFAs与FFA耐受菌株表面的结合减少。此外,WTA上缺乏GlcNAc赋予了对酸胁迫的耐受性。总之,这些发现支持WTA的GlcNAc修饰在[具体病原体名称未给出]对作为腐生菌和病原体生长过程中遇到的应激条件(包括富含FFA的环境)的反应中起重要作用。最重要的是,我们的数据表明,WTA上缺乏GlcNAc的[具体病原体名称未给出]菌株受到FFA毒性的保护,因为FFAs从缺乏GlcNAc的菌株的细菌表面被排斥。

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