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代谢相互作用控制了质粒编码的抗生素耐药性在表面相关微生物生长过程中的转移和传播。

Metabolic interactions control the transfer and spread of plasmid-encoded antibiotic resistance during surface-associated microbial growth.

机构信息

Department of Environmental Microbiology, Swiss Federal Institute of Aquatic Science and Technology (Eawag), 8600 Dübendorf, Switzerland; Department of Environmental Systems Science, Swiss Federal Institute of Technology (ETH), 8092 Zürich, Switzerland.

Department of Materials, Swiss Federal Institute of Technology (ETH), 8093 Zürich, Switzerland.

出版信息

Cell Rep. 2024 Sep 24;43(9):114653. doi: 10.1016/j.celrep.2024.114653. Epub 2024 Aug 30.

DOI:10.1016/j.celrep.2024.114653
PMID:39213158
Abstract

Surface-associated microbial systems are hotspots for the spread of plasmid-encoded antibiotic resistance, but how surface association affects plasmid transfer and proliferation remains unclear. Surface association enables prolonged spatial proximities between different populations, which promotes plasmid transfer between them. However, surface association also fosters strong metabolic interactions between different populations, which can direct their spatial self-organization with consequences for plasmid transfer and proliferation. Here, we hypothesize that metabolic interactions direct the spatial self-organization of different populations and, in turn, regulate the spread of plasmid-encoded antibiotic resistance. We show that resource competition causes populations to spatially segregate, which represses plasmid transfer. In contrast, resource cross-feeding causes populations to spatially intermix, which promotes plasmid transfer. We further show that the spatial positionings that emerge from metabolic interactions determine the proliferation of plasmid recipients. Our results demonstrate that metabolic interactions are important regulators of both the transfer and proliferation of plasmid-encoded antibiotic resistance.

摘要

表面相关的微生物系统是质粒编码的抗生素耐药性传播的热点,但表面关联如何影响质粒的转移和增殖仍不清楚。表面关联使不同种群之间的空间接近度延长,从而促进它们之间的质粒转移。然而,表面关联也促进了不同种群之间强烈的代谢相互作用,这可以指导它们的空间自组织,从而影响质粒的转移和增殖。在这里,我们假设代谢相互作用指导不同种群的空间自组织,并反过来调节质粒编码的抗生素耐药性的传播。我们表明,资源竞争导致种群空间隔离,从而抑制质粒转移。相比之下,资源交叉喂养导致种群空间混合,从而促进质粒转移。我们进一步表明,代谢相互作用产生的空间定位决定了质粒受体的增殖。我们的结果表明,代谢相互作用是质粒编码的抗生素耐药性转移和增殖的重要调节剂。

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