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AmrZ 通过 c-di-GMP 调节恶臭假单胞菌 F113 细胞外基质成分。

Regulation of extracellular matrix components by AmrZ is mediated by c-di-GMP in Pseudomonas ogarae F113.

机构信息

Departamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Darwin, 2, 28049, Madrid, Spain.

Department of Fundamental Microbiology, University of Lausanne, 1015, Lausanne, Switzerland.

出版信息

Sci Rep. 2022 Jul 13;12(1):11914. doi: 10.1038/s41598-022-16162-x.

Abstract

The AmrZ/FleQ hub has been identified as a central node in the regulation of environmental adaption in the plant growth-promoting rhizobacterium and model for rhizosphere colonization Pseudomonas ogarae F113. AmrZ is involved in the regulation of motility, biofilm formation, and bis-(3'-5')-cyclic dimeric guanosine monophosphate (c-di-GMP) turnover, among others, in this bacterium. The mutants in amrZ have a pleiotropic phenotype with distinguishable colony morphology, reduced biofilm formation, increased motility, and are severely impaired in competitive rhizosphere colonization. Here, RNA-Seq and qRT-PCR gene expression analyses revealed that AmrZ regulates many genes related to the production of extracellular matrix (ECM) components at the transcriptional level. Furthermore, overproduction of c-di-GMP in an amrZ mutant, by ectopic production of the Caulobacter crescentus constitutive diguanylate cyclase PleD*, resulted in increased expression of many genes implicated in the synthesis of ECM components. The overproduction of c-di-GMP in the amrZ mutant also suppressed the biofilm formation and motility phenotypes, but not the defect in competitive rhizosphere colonization. These results indicate that although biofilm formation and motility are mainly regulated indirectly by AmrZ, through the modulation of c-di-GMP levels, the implication of AmrZ in rhizosphere competitive colonization occurs in a c-di-GMP-independent manner.

摘要

AmrZ/FleQ 枢纽被鉴定为植物促生根际细菌和根际定殖模式假单胞菌 Ogarae F113 中环境适应调节的中心节点。AmrZ 参与调节该细菌的运动性、生物膜形成和双-(3'-5')-环二鸟苷单磷酸 (c-di-GMP) 周转等。amrZ 突变体具有表型多效性,菌落形态可区分,生物膜形成减少,运动性增加,在竞争根际定殖中严重受损。在这里,RNA-Seq 和 qRT-PCR 基因表达分析表明,AmrZ 在转录水平上调节许多与细胞外基质 (ECM) 成分产生相关的基因。此外,通过异位产生 Caulobacter crescentus 组成型二鸟苷酸环化酶 PleD*,在 amrZ 突变体中过量产生 c-di-GMP,导致许多与 ECM 成分合成相关的基因表达增加。amrZ 突变体中 c-di-GMP 的过度产生也抑制了生物膜形成和运动性表型,但没有抑制竞争根际定殖的缺陷。这些结果表明,尽管生物膜形成和运动性主要通过 AmrZ 间接调节,通过调节 c-di-GMP 水平,但 AmrZ 参与根际竞争定殖的情况以 c-di-GMP 独立的方式发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3836/9279365/dfe71a2e6819/41598_2022_16162_Fig1_HTML.jpg

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