plant microbe interaction
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Trends in Plant Science: Susceptibility to plant disease: more than a failure of host immunity (2013)

Trends in Plant Science: Susceptibility to plant disease: more than a failure of host immunity (2013) | plant microbe interaction | Scoop.it

Susceptibility to infectious diseases caused by pathogens affects most plants in their natural habitat and leads to yield losses in agriculture. However, plants are not helpless because their immune system can deal with the vast majority of attackers. Nevertheless, adapted pathogens are able to circumvent or avert host immunity making plants susceptible to these uninvited guests. In addition to the failure of the plant immune system, there are other host processes that contribute to plant disease susceptibility. In this review, we discuss recent studies that show the active role played by the host in supporting disease, focusing mainly on biotrophic stages of infection. Plants attract pathogens, enable their entry and accommodation, and facilitate nutrient provision.


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PLOS Pathogens: An RxLR Effector from Phytophthora infestans Prevents Re-localisation of Two Plant NAC Transcription Factors from the Endoplasmic Reticulum to the Nucleus (2013)

PLOS Pathogens: An RxLR Effector from Phytophthora infestans Prevents Re-localisation of Two Plant NAC Transcription Factors from the Endoplasmic Reticulum to the Nucleus (2013) | plant microbe interaction | Scoop.it

The potato late blight pathogen Phytophthora infestans secretes an array of effector proteins thought to act in its hosts by disarming defences and promoting pathogen colonisation. However, little is known about the host targets of these effectors and how they are manipulated by the pathogen. This work describes the identification of two putative membrane-associated NAC transcription factors (TF) as the host targets of the RxLR effector PITG_03192 (Pi03192). The effector interacts with NAC Targeted by Phytophthora (NTP) 1 and NTP2 at the endoplasmic reticulum (ER) membrane, where these proteins are localised. Transcripts of NTP1 and NTP2 rapidly accumulate following treatment with culture filtrate (CF) from in vitro grown P. infestans, which acts as a mixture of Phytophthora PAMPs and elicitors, but significantly decrease during P. infestans infection, indicating that pathogen activity may prevent their up-regulation. Silencing of NTP1 or NTP2 in the model host plant Nicotiana benthamiana increases susceptibility to P. infestans, whereas silencing of Pi03192 in P. infestans reduces pathogenicity. Transient expression of Pi03192 in planta restores pathogenicity of the Pi03192-silenced line. Moreover, colonisation by the Pi03192-silenced line is significantly enhanced on N. benthamiana plants in which either NTP1 or NTP2 have been silenced. StNTP1 and StNTP2 proteins are released from the ER membrane following treatment with P. infestans CF and accumulate in the nucleus, after which they are rapidly turned over by the 26S proteasome. In contrast, treatment with the defined PAMP flg22 fails to up-regulate NTP1 and NTP2, or promote re-localisation of their protein products to the nucleus, indicating that these events follow perception of a component of CF that appears to be independent of the FLS2/flg22 pathway. Importantly, Pi03192 prevents CF-triggered re-localisation of StNTP1 and StNTP2 from the ER into the nucleus, revealing a novel effector mode-of-action to promote disease progression.


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Video: Aphids responding to alarm pheromone (2011)

This clip shows aphids (Myzus persicae on Chinese cabbage) responding to alarm pheromone. A colony is on a leaf, a syringe delivers some alarm pheromone (you can just about see it at the start of the clip). After perceiving the alarm pheromone, the aphids become agitated and move away. Video by Christine Woodcock.


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PLOS ONE: The Pseudomonas syringae pv. tomato Type III Effector HopM1 Suppresses Arabidopsis Defenses Independent of Suppressing Salicylic Acid Signaling and of Targeting AtMIN7 (2013)

PLOS ONE: The Pseudomonas syringae pv. tomato Type III Effector HopM1 Suppresses Arabidopsis Defenses Independent of Suppressing Salicylic Acid Signaling and of Targeting AtMIN7 (2013) | plant microbe interaction | Scoop.it

Pseudomonas syringae pv tomato strain DC3000 (Pto) delivers several effector proteins promoting virulence, including HopM1, into plant cells via type III secretion. HopM1 contributes to full virulence of Pto by inducing degradation of Arabidopsis proteins, including AtMIN7, an ADP ribosylation factor-guanine nucleotide exchange factor. Pseudomonas syringae pvphaseolicola strain NPS3121 (Pph) lacks a functional HopM1 and elicits robust defenses inArabidopsis thaliana, including accumulation of pathogenesis related 1 (PR-1) protein and deposition of callose-containing cell wall fortifications. We have examined the effects of heterologously expressed HopM1Pto on Pph-induced defenses. HopM1 suppresses Pph-induced PR-1 expression, a widely used marker for salicylic acid (SA) signaling and systemic acquired resistance. Surprisingly, HopM1 reduces PR-1 expression without affecting SA accumulation and also suppresses the low levels of PR-1 expression apparent in SA-signaling deficient plants. Further, HopM1 enhances the growth of Pto in SA-signaling deficient plants. AtMIN7 contributes to Pph-induced PR-1 expression. However, HopM1 fails to degrade AtMIN7 during Pph infection and suppresses Pph-induced PR-1 expression and callose deposition in wild-type and atmin7 plants. We also show that the HopM1-mediated suppression of PR-1 expression is not observed in plants lacking the TGA transcription factor, TGA3. Our data indicate that HopM1 promotes bacterial virulence independent of suppressing SA-signaling and links TGA3, AtMIN7, and other HopM1 targets to pathways distinct from the canonical SA-signaling pathway contributing to PR-1 expression and callose deposition. Thus, efforts to understand this key effector must consider multiple targets and unexpected outputs of its action.


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New Phytologist: The Pseudomonas syringae type III effector HopD1 suppresses effector-triggered immunity, localizes to the endoplasmic reticulum, and targets the Arabidopsis transcription factor NT...

New Phytologist: The Pseudomonas syringae type III effector HopD1 suppresses effector-triggered immunity, localizes to the endoplasmic reticulum, and targets the Arabidopsis transcription factor NT... | plant microbe interaction | Scoop.it

Pseudomonas syringae type III effectors are known to suppress plant immunity to promote bacterial virulence. However, the activities and targets of these effectors are not well understood.We used genetic, molecular, and cell biology methods to characterize the activities, localization, and target of the HopD1 type III effector in Arabidopsis.HopD1 contributes to P. syringae virulence in Arabidopsis and reduces effector-triggered immunity (ETI) responses but not pathogen-associated molecular pattern-triggered immunity (PTI) responses. Plants expressing HopD1 supported increased growth of ETI-inducing P. syringae strains compared with wild-type Arabidopsis. We show that HopD1 interacts with the membrane-tethered Arabidopsis transcription factor NTL9 and demonstrate that this interaction occurs at the endoplasmic reticulum (ER). A P. syringae hopD1 mutant and ETI-inducing P. syringae strains exhibited enhanced growth on Arabidopsis ntl9 mutant plants. Conversely, growth of P. syringae strains was reduced in plants expressing a constitutively active NTL9 derivative, indicating that NTL9 is a positive regulator of plant immunity. Furthermore, HopD1 inhibited the induction of NTL9-regulated genes during ETI but not PTI.HopD1 contributes to P. syringae virulence in part by targeting NTL9, resulting in the suppression of ETI responses but not PTI responses and the promotion of plant pathogenicity.


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PNAS: Chitin-induced activation of immune signaling by the rice receptor CEBiP relies on a unique sandwich-type dimerization (2014)

PNAS: Chitin-induced activation of immune signaling by the rice receptor CEBiP relies on a unique sandwich-type dimerization (2014) | plant microbe interaction | Scoop.it

Perception of microbe-associated molecular patterns (MAMPs) through pattern recognition receptors (PRRs) triggers various defense responses in plants. This MAMP-triggered immunity plays a major role in the plant resistance against various pathogens. To clarify the molecular basis of the specific recognition of chitin oligosaccharides by the rice PRR, CEBiP (chitin-elicitor binding protein), as well as the formation and activation of the receptor complex, biochemical, NMR spectroscopic, and computational studies were performed. Deletion and domain-swapping experiments showed that the central lysine motif in the ectodomain of CEBiP is essential for the binding of chitin oligosaccharides. Epitope mapping by NMR spectroscopy indicated the preferential binding of longer-chain chitin oligosaccharides, such as heptamer-octamer, to CEBiP, and also the importance of N-acetyl groups for the binding. Molecular modeling/docking studies clarified the molecular interaction between CEBiP and chitin oligosaccharides and indicated the importance of Ile122 in the central lysine motif region for ligand binding, a notion supported by site-directed mutagenesis. Based on these results, it was indicated that two CEBiP molecules simultaneously bind to one chitin oligosaccharide from the opposite side, resulting in the dimerization of CEBiP. The model was further supported by the observations that the addition of (GlcNAc)8 induced dimerization of the ectodomain of CEBiP in vitro, and the dimerization and (GlcNAc)8-induced reactive oxygen generation were also inhibited by a unique oligosaccharide, (GlcNβ1,4GlcNAc)4, which is supposed to have N-acetyl groups only on one side of the molecule. Based on these observations, we proposed a hypothetical model for the ligand-induced activation of a receptor complex, involving both CEBiP and Oryza sativa chitin-elicitor receptor kinase-1.


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Science: Structural Basis for flg22-Induced Activation of the Arabidopsis FLS2-BAK1 Immune Complex (2013)

Science: Structural Basis for flg22-Induced Activation of the Arabidopsis FLS2-BAK1 Immune Complex (2013) | plant microbe interaction | Scoop.it

Flagellin perception in Arabidopsis is through recognition of its highly conserved N-terminal epitope (flg22) by flagellin-sensitive 2 (FLS2). Flg22 binding induces FLS2 heteromerization with BRI1-associated kinase 1 (BAK1) and their reciprocal activation followed by plant immunity. Here, we report the crystal structure of FLS2 and BAK1 ectodomains complexed with flg22 at 3.06 angstroms. A conserved and a nonconserved site from the inner surface of the FLS2 solenoid recognize the C- and N-terminal segment of flg22, respectively, without oligomerization or conformational changes in the FLS2 ectodomain. Besides directly interacting with FLS2, BAK1 acts as a coreceptor by recognizing the C terminus of the FLS2-bound flg22. Our data reveal the molecular mechanisms underlying FLS2-BAK1 complex recognition of flg22 and provide insight into the immune receptor complex activation.


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Frontiers in Plant-Microbe Interaction: Characterization of cell death inducing Phytophthora capsici CRN effectors suggests diverse activities in the host nucleus (2013)

Frontiers in Plant-Microbe Interaction: Characterization of cell death inducing Phytophthora capsici CRN effectors suggests diverse activities in the host nucleus (2013) | plant microbe interaction | Scoop.it

Plant-Microbe interactions are complex associations that feature recognition of Pathogen Associated Molecular Patterns by the plant immune system and dampening of subsequent responses by pathogen encoded secreted effectors. With large effector repertoires now identified in a range of sequenced microbial genomes, much attention centers on understanding their roles in immunity or disease. These studies not only allow identification of pathogen virulence factors and strategies, they also provide an important molecular toolset suited for studying immunity in plants. The Phytophthora intracellular effector repertoire encodes a large class of proteins that translocate into host cells and exclusively target the host nucleus. Recent functional studies have implicated the CRN protein family as an important class of diverse effectors that target distinct subnuclear compartments and modify host cell signaling. Here, we characterized three necrosis inducing CRNs and show that there are differences in the levels of cell death. We show that only expression of CRN20_624 has an additive effect on PAMP induced cell death but not AVR3a induced ETI. Given their distinctive phenotypes, we assessed localization of each CRN with a set of nuclear markers and found clear differences in CRN subnuclear distribution patterns. These assays also revealed that expression of CRN83_152 leads to a distinct change in nuclear chromatin organization, suggesting a distinct series of events that leads to cell death upon over-expression. Taken together, our results suggest diverse functions carried by CRN C-termini, which can be exploited to identify novel processes that take place in the host nucleus and are required for immunity or susceptibility.


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Video: Xanthomonas-plant interactions (2012)


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Abigail Rumsey's comment, November 13, 2013 10:46 AM
Very cool. This would be good to explain how plant diseases work even to people that don't know anything about plant pathology (if you took out all of the highly scientific words!).
Teresa M. Nash's comment, November 28, 2013 1:34 AM
thanks for this.
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Nature Communications: Effectors of animal and plant pathogens use a common domain to bind host phosphoinositides (2013)

Nature Communications: Effectors of animal and plant pathogens use a common domain to bind host phosphoinositides (2013) | plant microbe interaction | Scoop.it

Bacterial Type III Secretion Systems deliver effectors into host cells to manipulate cellular processes to the advantage of the pathogen. Many host targets of these effectors are found on membranes. Therefore, to identify their targets, effectors often use specialized membrane-localization domains to localize to appropriate host membranes. However, the molecular mechanisms used by many domains are unknown. Here we identify a conserved bacterial phosphoinositide-binding domain (BPD) that is found in functionally diverse Type III effectors of both plant and animal pathogens. We show that members of the BPD family functionally bind phosphoinositides and mediate localization to host membranes. Moreover, NMR studies reveal that the BPD of the newly identified Vibrio parahaemolyticus Type III effector VopR is unfolded in solution, but folds into a specific structure upon binding its ligand phosphatidylinositol-(4,5)-bisphosphate. Thus, our findings suggest a possible mechanism for promoting refolding of Type III effectors after delivery into host cells.


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MPMI: Effectors as tools in disease resistance breeding against biotrophic, hemi-biotrophic and necrotrophic plant pathogens (2014)

MPMI: Effectors as tools in disease resistance breeding against biotrophic, hemi-biotrophic and necrotrophic plant pathogens (2014) | plant microbe interaction | Scoop.it

One of most important challenges in plant breeding is improving resistance to the plethora of pathogens that threaten our crops. The ever growing world population, changing pathogen populations and fungicide resistance issues have increased the urgency of this task. In addition to a vital inflow of novel resistance sources into breeding programmes, the functional characterisation and deployment of resistance also needs improvement. Plant breeders therefore need to adopt new strategies and techniques. In modern resistance breeding, effectors are emerging as tools to accelerate and improve the identification, functional characterisation and deployment of R genes. Since genome-wide catalogues of effectors have become available for various pathogens, including biotrophs as well as necrotrophs, effector-assisted breeding has been shown to be successful for various crops. “Effectoromics” has contributed to classical resistance breeding as well as for GM approaches. Here we present an overview of how effector-assisted breeding and deployment is being exploited for various pathosystems.


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