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化学相互作用和互补适应策略转换细菌拮抗和共存。

Chemical interplay and complementary adaptative strategies toggle bacterial antagonism and co-existence.

机构信息

Instituto de Hortofruticultura Subtropical y Mediterránea "La Mayora," Universidad de Málaga-Consejo Superior de Investigaciones Científicas (IHSM-UMA-CSIC), Departamento de Microbiología, Universidad de Málaga, Bulevar Louis Pasteur 31 (Campus Universitario de Teatinos), 29071 Málaga, Spain.

University of California San Diego, Scripps Institution of Oceanography, La Jolla, CA, USA; University of California San Diego, Collaborative Mass Spectrometry Innovation Center, La Jolla, CA, USA.

出版信息

Cell Rep. 2021 Jul 27;36(4):109449. doi: 10.1016/j.celrep.2021.109449.

DOI:10.1016/j.celrep.2021.109449
PMID:34320359
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8333196/
Abstract

Bacterial communities are in a continuous adaptive and evolutionary race for survival. In this work we expand our knowledge on the chemical interplay and specific mutations that modulate the transition from antagonism to co-existence between two plant-beneficial bacteria, Pseudomonas chlororaphis PCL1606 and Bacillus amyloliquefaciens FZB42. We reveal that the bacteriostatic activity of bacillaene produced by Bacillus relies on an interaction with the protein elongation factor FusA of P. chlororaphis and how mutations in this protein lead to tolerance to bacillaene and other protein translation inhibitors. Additionally, we describe how the unspecific tolerance of B. amyloliquefaciens to antimicrobials associated with mutations in the glycerol kinase GlpK is provoked by a decrease of Bacillus cell membrane permeability, among other pleiotropic responses. We conclude that nutrient specialization and mutations in basic biological functions are bacterial adaptive dynamics that lead to the coexistence of two primary competitive bacterial species rather than their mutual eradication.

摘要

细菌群落为了生存而进行着持续的适应性和进化竞赛。在这项工作中,我们扩展了对两种植物有益细菌——荧光假单胞菌 PCL1606 和解淀粉芽孢杆菌 FZB42 之间从拮抗到共存转变的化学相互作用和特定突变的认识。我们揭示了芽孢杆菌产生的杆菌肽的抑菌活性依赖于与荧光假单胞菌的蛋白延伸因子 FusA 的相互作用,以及该蛋白中的突变如何导致对杆菌肽和其他蛋白翻译抑制剂的耐受。此外,我们描述了解淀粉芽孢杆菌对与甘油激酶 GlpK 突变相关的抗生素的非特异性耐受是如何通过降低芽孢杆菌细胞膜通透性等多种表型反应引起的。我们得出的结论是,营养专业化和基本生物功能的突变是导致两种主要竞争细菌共存而不是相互消灭的细菌适应动态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/53b50bde559f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/d7e3410fe02e/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/373b5b54acb0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/53e3c822360a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/09fe3a55a954/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/ed551001fdf7/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/b3387d503bcd/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/53b50bde559f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/d7e3410fe02e/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/373b5b54acb0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/53e3c822360a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/09fe3a55a954/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/ed551001fdf7/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/b3387d503bcd/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f3/8333196/53b50bde559f/gr6.jpg

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