Pathogen effector recognition-dependent association of NRG1 with EDS1 and SAG101 in TNL receptor immunity

Sun, Xinhua; Lapin, Dmitry; Feehan, Joanna M.; Stolze, Sara C.; Kramer, Katharina; Dongus, Joram A; Rzemieniewski, Jakub; Blanvillain-Baufumé, Servane; Harzen, Anne; Bautor, Jaqueline; Derbyshire, Paul; Menke, Frank L. H.; Finkemeier, Iris; Nakagami, Hirofumi; Jones, Jonathan D. G.; Parker, Jane E.

doi:10.1038/s41467-021-23614-x

Cited by 133 publications

(228 citation statements)

References 70 publications

Supporting

Mentioning

208

Contrasting

Order By: Relevance

“…For example, many tested TNLs, including RPS4:RRS1, RPP2, WRR4A, SNC1 and SOC3:CHS1, require contributions from both NRG1 and ADR1 family proteins (Dong et al 2016;Wu et al 2019;Saile et al 2020). On the other hand, ETI initiated by RPP4 and CNLs, such as RPS2 and RPS5, is mostly dependent on ADR1 family members (Dong et al 2016;Castel et al 2019;Wu et al 2019;Sun et al 2021). Additionally, NRG1.3, which lacks the CC R domain and is not directly involved in disease resistance (Wu et al 2019), may act as a negative regulator of defence signalling through interaction with the EDS1 family members (Sun et al 2021).…”

Section: Downstream Pathways-the Eds1 Family and Helper Rnls Control Immune Signalling Activated By Tnls And Some Cnlsmentioning

confidence: 99%

“…In addition, gymnosperms and angiosperms have acquired lipase-like proteins that belong to the EDS1 (enhanced disease susceptibility 1) family, which are involved in a broad range of plant innate immune responses (Lapin et al 2020 ). Recent studies suggest that the EDS1 family members likely relay signals from activated sensor NLRs to helper NLRs (Sun et al 2021 ; Wu et al 2021 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Structural basis of NLR activation and innate immune signalling in plants

et al. 2022

View full text Add to dashboard Cite

Animals and plants have NLRs (nucleotide-binding leucine-rich repeat receptors) that recognize the presence of pathogens and initiate innate immune responses. In plants, there are three types of NLRs distinguished by their N-terminal domain: the CC (coiled-coil) domain NLRs, the TIR (Toll/interleukin-1 receptor) domain NLRs and the RPW8 (resistance to powdery mildew 8)-like coiled-coil domain NLRs. CC-NLRs (CNLs) and TIR-NLRs (TNLs) generally act as sensors of effectors secreted by pathogens, while RPW8-NLRs (RNLs) signal downstream of many sensor NLRs and are called helper NLRs. Recent studies have revealed three dimensional structures of a CNL (ZAR1) including its inactive, intermediate and active oligomeric state, as well as TNLs (RPP1 and ROQ1) in their active oligomeric states. Furthermore, accumulating evidence suggests that members of the family of lipase-like EDS1 (enhanced disease susceptibility 1) proteins, which are uniquely found in seed plants, play a key role in providing a link between sensor NLRs and helper NLRs during innate immune responses. Here, we summarize the implications of the plant NLR structures that provide insights into distinct mechanisms of action by the different sensor NLRs and discuss plant NLR-mediated innate immune signalling pathways involving the EDS1 family proteins and RNLs.

show abstract

Section: Downstream Pathways-the Eds1 Family and Helper Rnls Control Immune Signalling Activated By Tnls And Some Cnlsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Structural basis of NLR activation and innate immune signalling in plants

et al. 2022

View full text Add to dashboard Cite

show abstract

“…TNL-mediated cell death and resistance requires a non-NLR protein, Enhanced Disease Susceptibility1 (EDS1) in Arabidopsis. EDS1 forms EDS1-SAG101 or EDS1-PAD4 complexes to determine the cell death and pathogen growth restriction respectively 63,64 , and EDS1-SAG101 engages with the RPW8-NLR NRG1 upon effector recognition 65 . Since the engineered NLR is RPS4-dependent, it is likely to signal via these modules.…”

Section: Discussionmentioning

confidence: 99%

Novel effector recognition capacity engineered into a paired NLR complex

Wang

Huang

Duxbury

et al. 2021

Preprint

Self Cite

View full text Add to dashboard Cite

The Arabidopsis RRS1-R Resistance gene confers recognition of the bacterial acetyltransferase PopP2 and another bacterial effector, AvrRps4. The RRS1-S allele recognizes AvrRps4 but not PopP2. RRS1-R/RRS1-S heterozygotes cannot recognize PopP2. RRS1-R and RRS1-S also suppress the constitutive RPS4-dependent autoactivity of RRS1-Rslh1. Phytoplasmas cause important plant diseases, and their effectors can cause degradation of specific host proteins. We tested whether attaching a pathogen effector-dependent degron to RRS1-R, enabling its degradation by phytoplasma effector SAP05, could derepress RRS1-Rslh1 autoactivity, resulting in SAP05-dependent resistance. In transient assays in tobacco, RRS1-R-derived constructs can confer a hypersensitive response (HR) to SAP05. However, phytoplasma infection assays in transgenic Arabidopsis resulted in delayed disease symptoms but not full resistance. We provide a proof-of-concept strategy utilizing the recessiveness of a plant immune receptor gene to engineer recognition of a pathogen effector that promotes degradation of a specific host protein.

show abstract

“…EDS1-PAD4 interacts with ADR1 type of RNLs to regulate basal immunity by transcriptionally modifying SA signaling pathway to induce local and systemic defense under TNL/ CNL-triggered ETI (Bonardi et al, 2011;Cui et al, 2017;Lapin et al, 2019;Saile et al, 2020). Recently, Sun et al (2021) showed that EDS1-PAD4-ADR1 and EDS1-SAG101-NRG1 constitute two separate immunity signaling nodes downstream of NLR activation to boost basal immunity against pathogens.…”

Section: Eds1: a Multitalented Defender Eds1 And Its Interacting Partners Trigger Distinct Pathwaysmentioning

confidence: 99%

Transcriptional Coactivators: Driving Force of Plant Immunity

et al. 2022

View full text Add to dashboard Cite

Salicylic acid (SA) is a plant defense signal that mediates local and systemic immune responses against pathogen invasion. However, the underlying mechanism of SA-mediated defense is very complex due to the involvement of various positive and negative regulators to fine-tune its signaling in diverse pathosystems. Upon pathogen infections, elevated level of SA promotes massive transcriptional reprogramming in which Non-expresser of PR genes 1 (NPR1) acts as a central hub and transcriptional coactivator in defense responses. Recent findings show that Enhanced Disease Susceptibility 1 (EDS1) also functions as a transcriptional coactivator and stimulates the expression of PR1 in the presence of NPR1 and SA. Furthermore, EDS1 stabilizes NPR1 protein level, while NPR1 sustains EDS1 expression during pathogenic infection. The interaction of NPR1 and EDS1 coactivators initiates transcriptional reprogramming by recruiting cyclin-dependent kinase 8 in the Mediator complex to control immune responses. In this review, we highlight the recent breakthroughs that considerably advance our understanding on how transcriptional coactivators interact with their functional partners to trigger distinct pathways to facilitate immune responses, and how SA accumulation induces dynamic changes in NPR1 structure for transcriptional reprogramming. In addition, the functions of different Mediator subunits in SA-mediated plant immunity are also discussed in light of recent discoveries. Taken together, the available evidence suggests that transcriptional coactivators are essential and potent regulators of plant defense pathways and play crucial roles in coordinating plant immune responses during plant–pathogen interactions.

show abstract

Pathogen effector recognition-dependent association of NRG1 with EDS1 and SAG101 in TNL receptor immunity

Cited by 133 publications

References 70 publications

Structural basis of NLR activation and innate immune signalling in plants

Structural basis of NLR activation and innate immune signalling in plants

Novel effector recognition capacity engineered into a paired NLR complex

Transcriptional Coactivators: Driving Force of Plant Immunity

Contact Info

Product

Resources

About