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PelD在环二鸟苷酸(c-di-GMP)下游对于鲁氏假单胞菌的宿主特异性是必需的。

PelD is required downstream of c-di-GMP for host specialization of Pseudomonas lurida.

作者信息

Czerwinski Anna, Löwenstrom Julia, Franzenburg Sören, Groth Espen Elias, Obeng Nancy, Schulenburg Hinrich

机构信息

Department of Evolutionary Ecology and Genetics, University of Kiel, 24118, Kiel, Germany.

Institute of Clinical Molecular Biology, University of Kiel, 24118, Kiel, Germany.

出版信息

BMC Microbiol. 2025 Apr 16;25(1):220. doi: 10.1186/s12866-025-03945-1.

Abstract

BACKGROUND

The bacterial second messenger c-di-GMP is known to influence the formation of biofilms and thereby persistence of pathogenic and beneficial bacteria in hosts. A previous evolution experiment with Pseudomonas lurida MYb11, occasional symbiont of the nematode Caenorhabditis elegans, led to the emergence of host-specialized variants with elevated intracellular c-di-GMP. Thus far, the molecular underpinnings of c-di-GMP-mediated host specialization were unknown in this symbiosis. Therefore, the current study aimed at identifying candidate molecular processes by combining transcriptomic and functional genetic analyses.

RESULTS

We found that MYb11 host specialists differentially expressed genes related to attachment, motility and biofilm production, including pelD from the pel gene cluster. pelD deletion resulted in reduced intra-host competitive fitness, lower bacterial numbers in C. elegans and loss of biofilm biomass.

CONCLUSION

Our results identify pelD as a previously unknown key modulator of beneficial symbiont-host associations that acts downstream of c-di-GMP.

摘要

背景

已知细菌第二信使环二鸟苷酸(c-di-GMP)会影响生物膜的形成,进而影响病原菌和有益菌在宿主体内的存活。先前对线虫秀丽隐杆线虫的偶然共生菌鲁氏假单胞菌MYb11进行的进化实验,导致出现了细胞内c-di-GMP水平升高的宿主特异性变体。迄今为止,在这种共生关系中,c-di-GMP介导的宿主特异性的分子基础尚不清楚。因此,本研究旨在通过结合转录组学和功能遗传学分析来鉴定候选分子过程。

结果

我们发现MYb11宿主特异性变体差异表达了与附着、运动和生物膜产生相关的基因,包括来自pel基因簇的pelD。pelD缺失导致宿主内竞争适应性降低、秀丽隐杆线虫体内细菌数量减少以及生物膜生物量损失。

结论

我们的结果确定pelD是一种先前未知的有益共生菌-宿主关联的关键调节因子,它在c-di-GMP下游发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/12001729/20912e6d2c1f/12866_2025_3945_Fig2_HTML.jpg

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