scholarly journals Phytophthora infestans RXLR-WY effector AVR3a associates with a Dynamin-Related Protein involved in endocytosis of a plant pattern recognition receptor

2014 ◽  
Author(s):  
Angela Chaparro-Garcia ◽  
Simon Schwizer ◽  
Jan Sklenar ◽  
Kentaro Yoshida ◽  
Jorunn I. B. Bos ◽  
...  
Keyword(s):  
Pattern Recognition ◽  
Cell Death ◽  
Phytophthora Infestans ◽  
Plant Pathogens ◽  
Defense Responses ◽  
Effector Proteins ◽  
Related Protein ◽  
Receptor Mediated Endocytosis ◽  
Molecular Patterns ◽  
Basal Immunity

Perception of pathogen associated molecular patterns (PAMPs) by cell surface localized pattern recognition receptors (PPRs), activates plant basal defense responses in a process known as PAMP/PRR–triggered immunity (PTI). In turn, pathogens deploy effector proteins that interfere with different steps in PTI signaling. However, our knowledge of PTI suppression by filamentous plant pathogens, i.e. fungi and oomycetes, remains fragmentary. Previous work revealed that BAK1/SERK3, a regulatory receptor of several PRRs, contributes to basal immunity against the Irish potato famine pathogen Phytophthora infestans. Moreover BAK1/SERK3 is required for the cell death induced by P. infestans elicitin INF1, a protein with characteristics of PAMPs. The P. infestans host-translocated RXLR-WY effector AVR3a is known to supress INF1-mediated defense by binding the E3 ligase CMPG1. In contrast, AVR3aKI-Y147del, a deletion mutant of the C-terminal tyrosine of AVR3a, fails to bind CMPG1 and suppress INF1 cell death. Here we studied the extent to which AVR3a and its variants perturb additional BAK1/SERK3 dependent PTI responses using the plant PRR FLAGELLIN SENSING 2 (FLS2). We found that all tested variants of AVR3a, including AVR3aKI-Y147del, suppress early defense responses triggered by the bacterial flagellin-derived peptide flg22 and reduce internalization of activated FLS2 from the plasma membrane without disturbing its nonactivated localization. Consistent with this effect of AVR3a on FLS2 endocytosis, we discovered that AVR3a associates with the Dynamin-Related Protein DRP2, a plant GTPase implicated in receptor-mediated endocytosis. Interestingly, DRP2 is required for ligand-induced FLS2 internalization but does not affect internalization of the growth receptor BRASSINOSTEROID INSENSITIVE 1 (BRI1). Furthermore, overexpression of DRP2 suppressed accumulation of reactive oxygen species triggered by PAMP treatment. We conclude that AVR3a associates with a key cellular trafficking and membrane-remodeling complex involved in immune receptor-mediated endocytosis and signaling. AVR3a is a multifunctional effector that can suppress BAK1/SERK3 mediated immunity through at least two different pathways.

scholarly journals Secretome Analysis and In Planta Expression of Salivary Proteins Identify Candidate Effectors from the Brown Planthopper Nilaparvata lugens

2019 ◽  
Vol 32 (2) ◽  
pp. 227-239 ◽  
Author(s):  
Weiwei Rao ◽  
Xiaohong Zheng ◽  
Bingfang Liu ◽  
Qin Guo ◽  
Jianping Guo ◽  
...  
Keyword(s):  
Cell Death ◽  
Expression Analysis ◽  
Plant Pathogens ◽  
Critical Role ◽  
Brown Planthopper ◽  
Ectopic Expression ◽  
Nilaparvata Lugens ◽  
Effector Proteins ◽  
Salivary Proteins ◽  
Secretome Analysis

The brown planthopper (BPH), Nilaparvata lugens (Stål), is a phloem sap-feeding insect. During feeding on rice plants, BPH secretes salivary proteins with potential effector functions, which may play a critical role in the plant–insect interactions. However, a limited number of BPH effector proteins have been identified to date. Here, we sequenced the salivary gland transcriptomes of five BPH populations and subsequently established a N. lugens secretome consisting of 1,140 protein-encoding genes. Secretome analysis revealed the presence of both conserved and rapidly evolving salivary proteins. A screen for potential effectors that elicit responses in the plant was performed via the transient expression analysis of 64 BPH salivary proteins in Nicotiana benthamiana leaves and rice protoplasts. The salivary proteins Nl12, Nl16, Nl28, and Nl43 induced cell death, whereas Nl40 induced chlorosis and Nl32 induced a dwarf phenotype in N. benthamiana, indicating effector properties of these proteins. Ectopic expression of the six salivary proteins in N. benthamiana upregulated expression of defense-related genes and callose deposition. Tissue expression analysis showed a higher expression level of the six candidate effectors in salivary glands than in other tissues. Subcellular localization and analysis of the domain required for cell death showed a diverse structure of the six effectors. Nl28, Nl40, and Nl43 are N. lugens specific; in contrast, Nl12, Nl16, and Nl32 are conserved among insects. The Nl40 family has numerous isoforms produced by alternative splicing, exemplifying rapid evolution and expansion of effector proteins in the BPH. Our results suggest a potential large effector repertoire in BPH and a higher level of effector conservation exist in BPH compared with that in plant pathogens.

Inhibitory pattern recognition receptors

2021 ◽  
Vol 219 (1) ◽  
Author(s):  
Matevž Rumpret ◽  
Helen J. von Richthofen ◽  
Victor Peperzak ◽  
Linde Meyaard
Keyword(s):  
Pattern Recognition ◽  
Cell Death ◽  
Immune System ◽  
Immune Responses ◽  
Pattern Recognition Receptors ◽  
Inhibitory Receptors ◽  
Danger Signals ◽  
Molecular Pattern ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Pathogen- and damage-associated molecular patterns are sensed by the immune system’s pattern recognition receptors (PRRs) upon contact with a microbe or damaged tissue. In situations such as contact with commensals or during physiological cell death, the immune system should not respond to these patterns. Hence, immune responses need to be context dependent, but it is not clear how context for molecular pattern recognition is provided. We discuss inhibitory receptors as potential counterparts to activating pattern recognition receptors. We propose a group of inhibitory pattern recognition receptors (iPRRs) that recognize endogenous and microbial patterns associated with danger, homeostasis, or both. We propose that recognition of molecular patterns by iPRRs provides context, helps mediate tolerance to microbes, and helps balance responses to danger signals.

scholarly journals Molecular mechanisms of host cell manipulation by plant pathogens

2014 ◽  
Vol 70 (a1) ◽  
pp. C801-C801
Author(s):  
Richard Hughes ◽  
Stuart King ◽  
Abbas Maqbool ◽  
Hazel McLellan ◽  
Tolga Bozkurt ◽  
...  
Keyword(s):  
Cell Death ◽  
Crop Production ◽  
Plant Pathogens ◽  
Molecular Mechanisms ◽  
Complex Structure ◽  
Effector Proteins ◽  
Plant Diseases ◽  
Cell Manipulation ◽  
Cell Physiology ◽  
Structural Studies

An estimated 15% of global crop production is lost to pre-harvest disease every year. New ways to manage plant diseases are required. A mechanistic understanding of how plant pathogens re-program their hosts to enable colonisation may provide novel genetic or chemical opportunities to interfere with disease. One notorious plant parasite is the Irish potato famine pathogen Phytophthora infestans. This pathogen remains a considerable threat to potato/tomato crops today as the agent of late blight. Plant pathogens secrete effector proteins outside of and into plant cells to suppress host defences and manipulate cell physiology. Structural studies have provided insights into effector evolution and enabled experiments to probe function [1-3]. Crystal structures of 4 Phytophthora RXLR-type effectors, which are unrelated in primary sequence, revealed similarities in the fold of these proteins. This fold was proposed to act as a stable scaffold that supports diversification of effectors. Further, molecular modelling has enabled mapping of single-site variants responsible for specialisation of a Phytophthora Cystatin-like effector, revealing how effectors can adapt to new hosts after a "host jump". Structural studies describing how RXLR-effectors interact with host targets are lacking. We have used Y2H/co-IP studies to identify host proteins that interact with P. infestans effectors PexRD2 and PexRD54. PexRD2 interacts with MAPKKKe, a component of plant immune signalling pathways, and suppressed cell death activities of this protein. We used the structure of PexRD2 to design mutants that fail to interact with MAPKKKe, and no longer suppress cell-death activities. We found that PexRD54 interacts with potato homologues of the autophagy protein ATG8. We have obtained a crystal structure for PexRD54 in the presence of ATG8. We are now using X-ray scattering to verify the complex structure in solution prior to establishing the role of this interaction during infection.

scholarly journals Genome-Wide Identification Reveals That Nicotiana benthamiana Hypersensitive Response (HR)-Like Lesion Inducing Protein 4 (NbHRLI4) Mediates Cell Death and Salicylic Acid-Dependent Defense Responses to Turnip Mosaic Virus

2021 ◽  
Vol 12 ◽  
Author(s):  
Xinyang Wu ◽  
Yuchao Lai ◽  
Shaofei Rao ◽  
Lanqing Lv ◽  
Mengfei Ji ◽  
...  
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Mosaic Virus ◽  
Hypersensitive Response ◽  
Nicotiana Benthamiana ◽  
Defense Responses ◽  
Turnip Mosaic Virus ◽  
Genome Wide ◽  
Transient Overexpression ◽  
Basal Immunity

Hypersensitive response (HR)-like cell death is an important mechanism that mediates the plant response to pathogens. In our previous study, we reported that NbHIR3s regulate HR-like cell death and basal immunity. However, the host genes involved in HR have rarely been studied. Here, we used transcriptome sequencing to identify Niben101Scf02063g02012.1, an HR-like lesion inducing protein (HRLI) in Nicotiana benthamiana that was significantly reduced by turnip mosaic virus (TuMV). HRLIs are uncharacterized proteins which may regulate the HR process. We identified all six HRLIs in N. benthamiana and functionally analyzed Niben101Scf02063g02012.1, named NbHRLI4, in response to TuMV. Silencing of NbHRLI4 increased TuMV accumulation, while overexpression of NbHRLI4 conferred resistance to TuMV. Transient overexpression of NbHRLI4 caused cell death with an increase in the expression of salicylic acid (SA) pathway genes but led to less cell death level and weaker immunity in plants expressing NahG. Thus, we have characterized NbHRLI4 as an inducer of cell death and an antiviral regulator of TuMV infection in a SA-mediated manner.

scholarly journals The ELR-SOBIR1 Complex Functions as a Two-Component Receptor-Like Kinase to Mount Defense Against Phytophthora infestans

2018 ◽  
Vol 31 (8) ◽  
pp. 795-802 ◽  
Author(s):  
Emmanouil Domazakis ◽  
Doret Wouters ◽  
Richard G. F. Visser ◽  
Sophien Kamoun ◽  
Matthieu H. A. J. Joosten ◽  
...  
Keyword(s):  
Cell Death ◽  
Phytophthora Infestans ◽  
Defense Responses ◽  
Virus Induced Gene Silencing ◽  
In Planta ◽  
Basal Resistance ◽  
Downstream Signaling ◽  
Receptor Like Kinase ◽  
Signaling Domain ◽  
Signaling Activation

The ELICITIN RESPONSE protein (ELR) from Solanum microdontum can recognize INF1 elicitin of Phytophthora infestans and trigger defense responses. ELR is a receptor-like protein (RLP) that lacks a cytoplasmic signaling domain and is anticipated to require interaction with a signaling-competent receptor-like kinase. SUPPRESSOR OF BIR1-1 (SOBIR1) has been proposed as a general interactor for RLPs involved in immunity and, as such, is a potential interactor for ELR. Here, we investigate whether SOBIR1 is required for response to INF1 and resistance to P. infestans and whether it associates with ELR. Our results show that virus-induced gene silencing of SOBIR1 in Nicotiana benthamiana leads to loss of INF1-triggered cell death and increased susceptibility to P. infestans. Using genetic complementation, we found that the kinase activity of SOBIR1 is required for INF1-triggered cell death. Coimmunoprecipitation experiments showed that ELR constitutively associates with potato SOBIR1 in planta, forming a bipartite receptor complex. Upon INF1 elicitation, this ELR-SOBIR1 complex recruits SERK3 (SOMATIC EMBRYOGENESIS RECEPTOR KINASE 3) leading to downstream signaling activation. Overall, our study shows that SOBIR1 is required for basal resistance to P. infestans and for INF1-triggered cell death and functions as an adaptor kinase for ELR.

scholarly journals Potato genotypes differentially alter the expression of Phytophthora infestans effectors during PAMP-mediated resistance induction

2019 ◽  
Author(s):  
Cécile Thomas ◽  
Pauline Le Boulch ◽  
Didier Andrivon ◽  
Florence Val
Keyword(s):  
Phytophthora Infestans ◽  
Induced Defense ◽  
Defense Responses ◽  
List Type ◽  
Defense Genes ◽  
Qrt Pcr ◽  
Effector Genes ◽  
Induced Defense Responses ◽  
Molecular Patterns ◽  
Kinetics Of

SummaryPathogen recognition by plants via pathogen-associated molecular patterns leads to PAMP-triggered immunity. However, pathogens can modulate it via the secretion of effectors. We hypothesize that in potato, induced defense triggered by a Phytophthora infestans concentrated culture filtrate (CCF) could alter both effector expression and disease severity.CCF was sprayed onto three potato genotypes with different resistance levels, before inoculation with P. infestans. Symptoms were scored visually at 1-4 dpi, while the expression of defense and effector genes was assessed by qRT-PCR.CCF induced most defense genes in Désirée (PRs, EIN3) and Bintje (PRs, PAL and POX), but repressed most defense genes in Rosafolia. On the contrary, CCF induced most effector genes in Rosafolia (Pi03192, Avrblb2, Avr3a, EPIC2B and SNE1). INF1 was over-expressed in Bintje, despite its earlier expression in both Désirée and Rosafolia compared to unsprayed controls. Pi03192 was repressed in Désirée, and was expressed earlier in Rosafolia than in controls. However, induced defense responses by CCF significantly reduced lesion areas at 3 dpi only in Désirée.The effectiveness of induced defense thus depends on host genotypes. It results from differential interactions and kinetics of defense and effector genes expressions.

Protein-protein interaction and molecular dynamics of Iturin A gene on effector proteins Phytophthora infestans

2020 ◽  
Vol 23 ◽  
Author(s):  
Bhimanagoud Kumbar ◽  
Shivananda Kandagalla ◽  
Bharath B R ◽  
Sharath B S ◽  
Riaz Mahmood
Keyword(s):  
Molecular Dynamics ◽  
Antifungal Activity ◽  
Phytophthora Infestans ◽  
Protein Interaction ◽  
In Silico ◽  
Plant Pathogens ◽  
Effector Proteins ◽  
P Value ◽  
Iturin A ◽  
Protein Protein Interaction

Aim And Objectives: Phytophthora infestans (Mont.) de Bary, fungal pathogen it causes late blight, which results in devastating economic loss among the Solanaceae. The bacillus lipopeptides shows the antagonistic activity against the many plant pathogens, among bacillus lipopeptides Iturin A reported as the antifungal gene. Hence, to understand the in silico antifungal activity, we have selected gene iturin A (AXN89987) produced by Bacillus spp to check the molecular dynamics study with the effector proteins of the P. infestanse. In this concern known effectors proteins of P. infestans were subjected to the protein-protein interaction and followed by simulation. Material and Method: Iturin A gene was amplified using the soil bacterium Bacillus subtilis with gene specific primers. Cloned into pTZ 57R/T vector and confirmed by sequencing. To get better insight the protein model was developed for Iturin A using Modeller 9.17, also for the effector proteins by using PDB structure of ID 4MRT (Phosphopantetheine Transferase Sfp) and 1QR0 (4'-phosphopantetheinyl moiety of coenzyme A) as template it shares the identity 72% and expected P-value: 3e-121 respectively. The model quality was assessed using ProSA and PROCHECK programs. Results: The potency of modelled protein against effector proteins of P. infestans were evaluated in silico using the HADDOCK server and the results showed the high affinity of Iturin A toward the effector protein Host ATG8 (PDB-5L83). Finally, the simulation was performed to the docked conformation of Iturin A with Host ATG8 to further understand the stability of the complex using Desmond program. Conclusion: Altogether the protein-protein interaction and simulation study propose a new methodology and intern it also attempted to uncover possible antifungal activity of iturin A against effector proteins of P. infestans.

scholarly journals Functional Interplay Between Two Xanthomonas oryzae pv. oryzae Secretion Systems in Modulating Virulence on Rice

2007 ◽  
Vol 20 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Gopaljee Jha ◽  
Ramanan Rajeshwari ◽  
Ramesh V. Sonti
Keyword(s):  
Cell Death ◽  
Double Mutant ◽  
Plant Pathogens ◽  
Substantial Reduction ◽  
Defense Responses ◽  
Xanthomonas Oryzae ◽  
Dependent Manner ◽  
Secretion Systems ◽  
Callose Deposition ◽  
Successful Infection

The type II (T2S) and type III (T3S) secretion systems are important for virulence of Xanthomonas oryzae pv. oryzae, causal agent of bacterial leaf blight of rice. The T3S of gram-negative bacterial plant pathogens has been shown to suppress host defense responses, including programmed cell death reactions, whereas the T2S is involved in secreting cell-wall-degrading enzymes. Here, we show that a T3S-deficient (T3S¯) mutant of X. oryzae pv. oryzae can induce a basal plant defense response seen as callose deposition, immunize rice against subsequent X. oryzae pv. oryzae infection, and cause cell-death-associated nuclear fragmentation. A T2S¯ T3S¯ double mutant exhibited a substantial reduction in the ability to evoke these responses. We purified two major effectors of the X. oryzae pv. oryzae T2S and characterized them to be a cellulase (ClsA) and a putative cellobiosidase (CbsA). The purified ClsA, CbsA, and lipase/esterase (LipA; a previously identified T2S effector) proteins induced rice defense responses that were suppressible by X. oryzae pv. oryzae in a T3S-dependent manner. These defense responses also were inducible by the products of the action of these purified proteins on rice cell walls. We further show that a CbsA¯ mutant or a ClsA¯ LipA¯ double mutant are severely virulence deficient. These results indicate that the X. oryzae pv. oryzae T2S secretes important virulence factors, which induce innate rice defense responses that are suppressed by T3S effectors to enable successful infection.

scholarly journals Viral fitness determines the magnitude of transcriptomic and epigenomic reprogramming of defense responses in plants

2019 ◽  
Author(s):  
Régis L. Corrêa ◽  
Alejandro Sanz-Carbonell ◽  
Zala Kogej ◽  
Sebastian Y. Müller ◽  
Sara López-Gomollón ◽  
...  
Keyword(s):  
Cytosine Methylation ◽  
Defense Responses ◽  
Infection Process ◽  
Viral Fitness ◽  
Antiviral Responses ◽  
Viral Adaptation ◽  
Stress Related Genes ◽  
Molecular Patterns ◽  
Basal Immunity ◽  
The Impact

SUMMARYAlthough epigenetic factors may influence the expression of defense genes in plants, their role in antiviral responses and the impact of viral adaptation and evolution in shaping these interactions are still poorly explored. We used two isolates of turnip mosaic potyvirus (TuMV) with varying degrees of adaptation to Arabidopsis thaliana to address these issues. One of the isolates was experimentally evolved in the plant and presented increased load and virulence relative to the ancestral isolate. The magnitude of the transcriptomic responses were larger for the evolved isolate and indicated a role of innate immunity systems triggered by molecular patterns and effectors in the infection process. Several transposable elements (TEs) located in different chromatin contexts and epigenetic-related genes were also affected. Correspondingly, mutant plants having loss or gain of repressive marks were, respectively, more tolerant and susceptible to TuMV, with a more efficient response against the ancestral isolate. In wild-type plants both isolates induced similar levels of cytosine methylation changes, including in and around TEs and stress-related genes. Results collectively suggested that apart from RNA silencing and basal immunity systems, DNA methylation and histone modification pathways may also be required for mounting proper antiviral defenses in plants and that the effectiveness of this type of regulation strongly depends on the degree of viral adaptation to the host.

Review: Soluble innate immune pattern-recognition proteins for clearing dying cells and cellular components: implications on exacerbating or resolving inflammation

2010 ◽  
Vol 16 (3) ◽  
pp. 191-200 ◽  
Author(s):  
Michael L. Litvack ◽  
Nades Palaniyar
Keyword(s):  
Pattern Recognition ◽  
Cell Death ◽  
Treatment Strategies ◽  
Innate Immune ◽  
Live Cells ◽  
Death Process ◽  
Clear Understanding ◽  
Phagocytic Cells ◽  
Molecular Patterns ◽  
Dying Cells

Soluble innate immune pattern-recognition proteins (sPRPs) identify non-self or altered-self molecular patterns. Dying cells often display altered-self arrays of molecules on their surfaces. Hence, sPRPs are ideal for recognizing these cells and their components. Dying cell surfaces often contain, or allow the access to different lipids, intracellular glycoproteins and nucleic acids such as DNA at different stages of cell death. These are considered as ‘eat me’ signals that replace the native ‘don’t eat me’ signals such as CD31, CD47 present on the live cells. A programmed cell death process such as apoptosis also generates cell surface blebs that contain intracellular components. These blebs are easily released for effective clearance or signalling. During late stages of cell death, soluble components are also released that act as ‘find me’ signal (e.g. LysoPC, nucleotides). The sPRPs such as collectins, ficolins, pentraxins, sCD14, MFG-E8, natural IgM and C1q can effectively identify some of these specific molecular patterns. The biological end-point is different depending on sPRP, tissue, stage of apoptosis and the type of cell death. The sPRPs that reside in the immune-privileged surfaces such as lungs often act as opsonins and enhance a silent clearance of dying cells and cellular material by macrophages and other phagocytic cells. Although the recognition of these materials by complement-activating proteins could amplify the opsonic signal, this pathway may aggravate inflammation. Clear understanding of the involvement of specific sPRPs in cell death and subsequent clearance of dying cell and their components is essential for devising appropriate treatment strategies for diseases involving infection, inflammation and auto-antibody generation.

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