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PSKR1 平衡了根际微生物组中的植物生长与防御权衡。

PSKR1 balances the plant growth-defence trade-off in the rhizosphere microbiome.

机构信息

Department of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.

Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA.

出版信息

Nat Plants. 2023 Dec;9(12):2071-2084. doi: 10.1038/s41477-023-01539-1. Epub 2023 Nov 16.

DOI:10.1038/s41477-023-01539-1
PMID:37973937
Abstract

Microbiota benefit their hosts by improving nutrient uptake and pathogen protection. How host immunity restricts microbiota while avoiding autoimmunity is poorly understood. Here we show that the Arabidopsis phytosulfokine receptor 1 (pskr1) mutant displays autoimmunity (plant stunting, defence-gene expression and reduced rhizosphere bacterial growth) in response to growth-promoting Pseudomonas fluorescens. Microbiome profiling and microbiota colonization showed that PSKR1-mediated reduction in bacterial growth and stunting is largely specific to Pseudomonas. Transcriptional profiling demonstrated that PSKR1 regulates the growth-defence trade-off during Pseudomonas colonization: PSKR1 upregulates plant photosynthesis and root growth but suppresses salicylic-acid-mediated defences. Genetic epistasis experiments showed that pskr1 stunting and restriction of bacterial growth are salicylic acid dependent. Finally, we showed that Pseudomonas, but not other bacteria, induces PSKR1 expression in roots, suggesting that Pseudomonas might manipulate plant signalling to promote its colonization. Our data demonstrate a genetic mechanism to coordinate beneficial functions of the microbiome while preventing autoimmunity.

摘要

微生物通过改善营养吸收和病原体保护来使宿主受益。然而,宿主免疫如何在限制微生物的同时避免自身免疫仍不清楚。在这里,我们发现拟南芥植物磺基丙氨酸受体 1 (pskr1) 突变体在响应促进生长的荧光假单胞菌时表现出自免疫(植物矮化、防御基因表达和根际细菌生长减少)。微生物组分析和微生物定植表明,PSKR1 介导的细菌生长和矮化减少在很大程度上是针对假单胞菌的。转录谱分析表明,PSKR1 在假单胞菌定植过程中调节生长-防御的权衡:PSKR1 上调植物光合作用和根生长,但抑制水杨酸介导的防御。遗传上位性实验表明,pskr1 矮化和细菌生长的限制依赖于水杨酸。最后,我们发现只有假单胞菌而不是其他细菌在根中诱导 PSKR1 的表达,这表明假单胞菌可能操纵植物信号以促进其定植。我们的数据证明了一种遗传机制,可协调微生物组的有益功能,同时防止自身免疫。

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