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再生诱导转录因子复合物 ERF115-PAT1 协调根结线虫诱导的根瘤中的创伤诱导反应。

The regeneration conferring transcription factor complex ERF115-PAT1 coordinates a wound-induced response in root-knot nematode induced galls.

机构信息

INRAE, Université Côte d'Azur, CNRS, ISA, Sophia Antipolis, 06903, France.

Federal University of Viçosa, Viçosa, MG, 36570-900, Brazil.

出版信息

New Phytol. 2024 Jan;241(2):878-895. doi: 10.1111/nph.19399. Epub 2023 Dec 3.

Abstract

The establishment of root-knot nematode (RKN; Meloidogyne spp.) induced galls in the plant host roots likely involves a wound-induced regeneration response. Confocal imaging demonstrates physical stress or injury caused by RKN infection during parasitism in the model host Arabidopsis thaliana. The ERF115-PAT1 heterodimeric transcription factor complex plays a recognized role in wound-induced regeneration. ERF115 and PAT1 expression flanks injured gall cells likely driving mechanisms of wound healing, implying a local reactivation of cell division which is also hypothetically involved in gall genesis. Herein, functional investigation revealed that ectopic ERF115 expression resulted in premature induction of galls, and callus formation adjacent to the expanding female RKN was seen upon PAT1 upregulation. Smaller galls and less reproduction were observed in ERF115 and PAT1 knockouts. Investigation of components in the ERF115 network upon overexpression and knockdown by qRT-PCR suggests it contributes to steer gall wound-sensing and subsequent competence for tissue regeneration. High expression of CYCD6;1 was detected in galls, and WIND1 overexpression resulted in similar ERF115 gall phenotypes, also showing faster gall induction. Along these lines, we show that the ERF115-PAT1 complex likely coordinates stress signalling with tissue healing, keeping the gall functional until maturation and nematode reproduction.

摘要

根结线虫(RKN;Meloidogyne spp.)在植物宿主根部形成根结可能涉及到创伤诱导的再生反应。共聚焦成像表明,在模式宿主拟南芥中寄生时,RKN 感染会导致物理应激或损伤。ERF115-PAT1 异二聚体转录因子复合物在创伤诱导的再生中发挥着公认的作用。ERF115 和 PAT1 的表达侧翼受伤的根结细胞可能驱动创伤愈合的机制,这意味着细胞分裂的局部重新激活,这也假设涉及根结的发生。在此,功能研究表明,异位表达 ERF115 导致根结的过早诱导,并且在 PAT1 上调时,在扩张的雌性 RKN 附近观察到愈伤组织的形成。在 ERF115 和 PAT1 敲除体中观察到根结更小且繁殖能力降低。通过 qRT-PCR 对 ERF115 网络的组成部分进行过表达和敲低的研究表明,它有助于引导根结创伤感应和随后的组织再生能力。在根结中检测到 CYCD6;1 的高表达,WIND1 的过表达导致类似的 ERF115 根结表型,也表现出更快的根结诱导。在这些方面,我们表明 ERF115-PAT1 复合物可能协调应激信号与组织愈合,使根结保持功能性,直到成熟和线虫繁殖。

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