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研究报道两个残基重编程固氮共生的免疫受体
作者:小柯机器人 发布时间:2025/11/6 21:14:25

奥尔胡斯大学Simona Radutoiu团队在研究中取得进展。他们报道了两个残基重编程固氮共生的免疫受体。2025年11月5日出版的《自然》发表了这项成果。

本研究表明,Nod因子受体NFR1细胞内部分的特定氨基酸残基控制信号特异性,并使免疫和共生反应得以区分。对CERK6、NFR1及其受体变体的功能研究发现,在激酶结构域的近膜区域存在一个保守的基元,研究人员将其称为共生决定因子1,这是共生信号传导的关键。该团队发现共生决定因子1中的两个残基是NFR1型受体不可缺少的标志,它们足以转化Lotthem CERK6和大麦RLK4激酶的输出,从而使Lotthem japonicthem的共生信号传导成为可能。

据介绍,受体信号传导决定细胞反应,对确定特定的生物学结果至关重要。在豆科植物根细胞中,当几丁质配体被感知时,高度相似且结构保守的几丁质和Nod因子受体激酶分别激活免疫或共生途径。

附:英文原文

Title: Two residues reprogram immunity receptors for nitrogen-fixing symbiosis

Author: Tsitsikli, Magdalini, Simonsen, Bine, Luu, Thi-Bich, Larsen, Maria M., Andersen, Camilla G., Gysel, Kira, Lironi, Damiano, Krnauer, Christina, Rbsam, Henriette, Hansen, Simon B., Brentsen, Ren, Wulff, Jesper Lundsgaard, Johansen, Sarah Holt, Sezer, Glendam, Stougaard, Jens, Andersen, Kasper Rjkjr, Radutoiu, Simona

Issue&Volume: 2025-11-05

Abstract: Receptor signalling determines cellular responses and is crucial for defining specific biological outcomes. In legume root cells, highly similar and structurally conserved chitin and Nod factor receptor kinases activate immune or symbiotic pathways, respectively, when chitinous ligands are perceived1. Here we show that specific amino acid residues in the intracellular part of the Nod factor receptor NFR1 control signalling specificity and enable the distinction of immune and symbiotic responses. Functional investigation of CERK6, NFR1 and receptor variants thereof revealed a conserved motif that we term Symbiosis Determinant 1 in the juxtamembrane region of the kinase domain, which is key for symbiotic signalling. We show that two residues in Symbiosis Determinant 1 are indispensable hallmarks of NFR1-type receptors and are sufficient to convert Lotus CERK6 and barley RLK4 kinase outputs to enable symbiotic signalling in Lotus japonicus.

DOI: 10.1038/s41586-025-09696-3

Source: https://www.nature.com/articles/s41586-025-09696-3

期刊信息

Nature:《自然》,创刊于1869年。隶属于施普林格·自然出版集团,最新IF:69.504
官方网址:http://www.nature.com/
投稿链接:http://www.nature.com/authors/submit_manuscript.html