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受体样激酶 SERK3/BAK1 是烟草原生质体对抗晚疫病菌(Phytophthora infestans)的基础抗性所必需的。

The receptor-like kinase SERK3/BAK1 is required for basal resistance against the late blight pathogen phytophthora infestans in Nicotiana benthamiana.

机构信息

The Sainsbury Laboratory, John Innes Centre, Norwich, United Kingdom.

出版信息

PLoS One. 2011 Jan 27;6(1):e16608. doi: 10.1371/journal.pone.0016608.

Abstract

BACKGROUND

The filamentous oomycete plant pathogen Phytophthora infestans causes late blight, an economically important disease, on members of the nightshade family (Solanaceae), such as the crop plants potato and tomato. The related plant Nicotiana benthamiana is a model system to study plant-pathogen interactions, and the susceptibility of N. benthamiana to Phytophthora species varies from susceptible to resistant. Little is known about the extent to which plant basal immunity, mediated by membrane receptors that recognise conserved pathogen-associated molecular patterns (PAMPs), contributes to P. infestans resistance.

PRINCIPAL FINDINGS

We found that different species of Phytophthora have varying degrees of virulence on N. benthamiana ranging from avirulence (incompatible interaction) to moderate virulence through to full aggressiveness. The leucine-rich repeat receptor-like kinase (LRR-RLK) BAK1/SERK3 is a major modulator of PAMP-triggered immunity (PTI) in Arabidopsis thaliana and N. benthamiana. We cloned two NbSerk3 homologs, NbSerk3A and NbSerk3B, from N. benthamiana based on sequence similarity to the A. thaliana gene. N. benthamiana plants silenced for NbSerk3 showed markedly enhanced susceptibility to P. infestans infection but were not altered in resistance to Phytophthora mirabilis, a sister species of P. infestans that specializes on a different host plant. Furthermore, silencing of NbSerk3 reduced the cell death response triggered by the INF1, a secreted P. infestans protein with features of PAMPs.

CONCLUSIONS/SIGNIFICANCE: We demonstrated that N. benthamiana NbSERK3 significantly contributes to resistance to P. infestans and regulates the immune responses triggered by the P. infestans PAMP protein INF1. In the future, the identification of novel surface receptors that associate with NbSERK3A and/or NbSERK3B should lead to the identification of new receptors that mediate recognition of oomycete PAMPs, such as INF1.

摘要

背景

丝状卵菌植物病原体致病疫霉引起晚疫病,这是一种经济上重要的疾病,发生在茄科(茄科)成员上,如作物马铃薯和番茄。相关植物烟草是研究植物-病原体相互作用的模式系统,而烟草对疫霉属物种的敏感性从易感性到抗性不等。对于由识别保守病原体相关分子模式(PAMPs)的膜受体介导的植物基础免疫在多大程度上有助于对致病疫霉的抗性,人们知之甚少。

主要发现

我们发现不同的疫霉物种对烟草的毒力程度不同,从无毒性(不亲和相互作用)到中度毒性,再到完全侵袭性。富含亮氨酸重复受体样激酶(LRR-RLK)BAK1/SERK3 是拟南芥和烟草中 PAMP 触发免疫(PTI)的主要调节因子。我们根据与拟南芥基因的序列相似性,从烟草中克隆了两个 NbSerk3 同源物,NbSerk3A 和 NbSerk3B。NbSerk3 沉默的烟草植物对致病疫霉感染的敏感性明显增强,但对同源种疫霉属 mirabilis 的抗性没有改变,疫霉属 mirabilis 是专门针对不同宿主植物的致病疫霉的姐妹种。此外,NbSerk3 的沉默降低了由 INF1 触发的细胞死亡反应,INF1 是一种分泌的致病疫霉蛋白,具有 PAMPs 的特征。

结论/意义:我们证明了烟草 NbSERK3 显著有助于对致病疫霉的抗性,并调节了由致病疫霉 PAMP 蛋白 INF1 触发的免疫反应。在未来,识别与 NbSERK3A 和/或 NbSERK3B 相关的新型表面受体,应该会导致鉴定出介导卵菌 PAMPs 识别的新受体,如 INF1。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc3d/3029390/f2cb655b7534/pone.0016608.g001.jpg

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