Plant immune signalling activated by the perception of pathogen‐associated molecular patterns (PAMPs) or effector proteins is mediated by pattern‐recognition receptors (PRRs) and nucleotide‐binding ...and leucine‐rich repeat domain‐containing receptors (NLRs), which often share cellular components and downstream responses. Many PRRs are leucine‐rich repeat receptor‐like kinases (LRR‐RLKs), which mostly perceive proteinaceous PAMPs. The suppressor of the G2 allele of skp1 (SGT1) is a core immune regulator required for the activation of NLR‐mediated immunity. In this work, we examined the requirement of SGT1 for immune responses mediated by several LRR‐RLKs in both Nicotiana benthamiana and Arabidopsis. Using complementary genetic approaches, we found that SGT1 is not limiting for early PRR‐dependent responses or antibacterial immunity. We therefore conclude that SGT1 does not play a significant role in bacterial PAMP‐triggered immunity.
Using complementary genetic approaches in both Nicotiana benthamiana and Arabidopsis, this article shows that SGT1 does not play a significant role in bacterial PAMP‐triggered LRR‐RLK‐mediated immunity.
The bacterial plant pathogenic
species belong to the beta-proteobacteria class and are soil-borne pathogens causing vascular bacterial wilt disease, affecting a wide range of plant hosts. These ...bacteria form a heterogeneous group considered as a "species complex" gathering three newly defined species. Like many other Gram negative plant pathogens,
pathogenicity relies on a type III secretion system, enabling bacteria to secrete/inject a large repertoire of type III effectors into their plant host cells. Type III-secreted effectors (T3Es) are thought to participate in generating a favorable environment for the pathogen (countering plant immunity and modifying the host metabolism and physiology).
Expert genome annotation, followed by specific type III-dependent secretion, allowed us to improve our Hidden-Markov-Model and Blast profiles for the prediction of type III effectors.
We curated the T3E repertoires of 12 plant pathogenic
strains, representing a total of 12 strains spread over the different groups of the species complex. This generated a pangenome repertoire of 102 T3E genes and 16 hypothetical T3E genes. Using this database, we scanned for the presence of T3Es in the 155 available genomes representing 140 distinct plant pathogenic
strains isolated from different host plants in different areas of the globe. All this information is presented in a searchable database. A presence/absence analysis, modulated by a strain sequence/gene annotation quality score, enabled us to redefine core and accessory T3E repertoires.
Summary
D14 and KAI2 receptors enable plants to distinguish between strigolactones (SLs) and karrikins (KARs), respectively, in order to trigger appropriate environmental and developmental responses. ...Both receptors are related to the regulation of arbuscular mycorrhiza (AM) formation and are members of the RsbQ‐like family of α,β‐hydrolases. DLK2 proteins, whose function remains unknown, constitute a third clade from the RsbQ‐like protein family. We investigated whether the tomato SlDLK2 is a new regulatory component in the AM symbiosis.
Genetic approaches were conducted to analyze SlDLK2 expression and to understand SlDLK2 function in AM symbiosis.
We show that SlDLK2 expression in roots is AM‐dependent and is associated with cells containing arbuscules. SlDLK2 ectopic expression arrests arbuscule branching and downregulates AM‐responsive genes, even in the absence of symbiosis; while the opposite effect was observed upon SlDLK2 silencing. Moreover, SlDLK2 overexpression in Medicago truncatula roots showed the same altered phenotype observed in tomato roots. Interestingly, SlDLK2 interacts with DELLA, a protein that regulates arbuscule formation/degradation in AM roots.
We propose that SlDLK2 is a new component of the complex plant‐mediated mechanism regulating the life cycle of arbuscules in AM symbiosis.
The soilborne bacterial pathogen Ralstonia solanacearum is one of the most destructive plant pathogens worldwide, and its infection process involves the manipulation of numerous plant cellular ...functions. In this work, we found that the R. solanacearum effector protein RipD partially suppressed different levels of plant immunity triggered by R. solanacearum elicitors, including specific responses triggered by pathogen‐associated molecular patterns and secreted effectors. RipD localized in different subcellular compartments in plant cells, including vesicles, and its vesicular localization was enriched in cells undergoing R. solanacearum infection, suggesting that this specific localization may be particularly relevant during infection. Among RipD‐interacting proteins, we identified plant vesicle‐associated membrane proteins (VAMPs). We also found that overexpression of Arabidopsis thaliana VAMP721 and VAMP722 in Nicotiana benthamiana leaves promoted resistance to R. solanacearum, and this was abolished by the simultaneous expression of RipD, suggesting that RipD targets VAMPs to contribute to R. solanacearum virulence. Among proteins secreted in VAMP721/722‐containing vesicles, CCOAOMT1 is an enzyme required for lignin biosynthesis, and mutation of CCOAOMT1 enhanced plant susceptibility to R. solanacearum. Altogether our results reveal the contribution of VAMPs to plant resistance against R. solanacearum and their targeting by a bacterial effector as a pathogen virulence strategy.
We found that the Ralstonia solanacearum type III effector RipD localize in vesicles in plant cells and targets vesicle‐associated membrane proteins to contribute to bacterial infection.
Jasmonate (JA) regulates various aspects of plant growth and development and stress responses, with prominent roles in male reproductive development and defenses against herbivores and necrotrophic ...pathogens. JASMONATE-ZIM DOMAIN (JAZ) proteins are key regulators in the JA signaling pathway and function to repress the expression of JA-responsive genes. Here, we show that JAZ proteins directly interact with several chromatin-associated Polycomb proteins to mediate repressive chromatin modifications at JA-responsive genes and, thus, their transcriptional repression in Arabidopsis. Genetic analyses revealed that the developmental defects, including anther and pollen abnormalities, resulting from loss or block of JA signaling were partially rescued by loss of Polycomb protein-mediated chromatin silencing (Polycomb repression). We further found that JAZ-mediated transcriptional repression during anther and pollen development requires Polycomb proteins at four key regulatory loci. Analysis of genome-wide occupancy of a Polycomb factor and transcriptome reprogramming in response to JA revealed that Polycomb repression is involved in the repression of various JA-responsive genes. Taken together, our study reveals an important chromatin-based mechanism for JAZ-mediated transcriptional repression and JA signaling in plants.
This study reports that JAZ proteins, the negative regulators of the jasmonate (JA) signaling pathway, directly interact and function together with chromatin-associated Polycomb factors to mediate repressive chromatin modifications and transcriptional repression at JA-responsive genes in Arabidopsis. This reveals a chromatin-based mechanism for JAZ-mediated transcriptional repression and JA signaling in plants.
is a devastating soil-borne bacterial pathogen that causes disease in multiple host plants worldwide. Typical assays to measure virulence of
in laboratory conditions rely on soil-drenching ...inoculation followed by observation and scoring of disease symptoms. Here, we describe a novel inoculation protocol to analyze the replication of
upon infiltration into the leaves of
, in which gene expression has been altered using
. The protocol includes five major steps: 1) growth of
plants; 2) infiltration of
; 3)
inoculation; 4) sample collection and bacterial quantitation; 5) data analysis and representation. The transient gene expression or gene silencing prior to
inoculation provides a straightforward way to perform genetic analysis of plant functions involved in the interaction between pathogen and host, using the appropriate combination of
and
strains, with high sensitivity and accuracy provided by the quantitation of bacterial numbers in plant tissues.
Plants establish mutualistic associations with beneficial microbes while deploying the immune system to defend against pathogenic ones. Little is known about the interplay between mutualism and ...immunity and the mediator molecules enabling such crosstalk. Here, we show that plants respond differentially to a volatile bacterial compound through integral modulation of the immune system and the phosphate‐starvation response (PSR) system, resulting in either mutualism or immunity. We found that exposure of Arabidopsis thaliana to a known plant growth‐promoting rhizobacterium can unexpectedly have either beneficial or deleterious effects to plants. The beneficial‐to‐deleterious transition is dependent on availability of phosphate to the plants and is mediated by diacetyl, a bacterial volatile compound. Under phosphate‐sufficient conditions, diacetyl partially suppresses plant production of reactive oxygen species (ROS) and enhances symbiont colonization without compromising disease resistance. Under phosphate‐deficient conditions, diacetyl enhances phytohormone‐mediated immunity and consequently causes plant hyper‐sensitivity to phosphate deficiency. Therefore, diacetyl affects the type of relation between plant hosts and certain rhizobacteria in a way that depends on the plant's phosphate‐starvation response system and phytohormone‐mediated immunity.
Synopsis
A volatile compound produced by a plant growth‐promoting rhizobacterium differentially affects phytohormone‐mediated immunity in phosphate‐sufficient and ‐deficient plants, thus modulating their response to symbiont colonization.
Exposure to a plant growth‐promoting rhizobacterium Bacillus amyloliquefaciens can cause either beneficial or deleterious effects on Arabidopsis thaliana plants depending on their nutrition status.
The beneficial vs. deleterious effects of the rhizobacterium depend on the availability of phosphate (Pi) to the plant.
The effect of the rhizobacterium on plant fitness is mediated by the volatile bacterial metabolite diacetyl (DA).
In Pi‐sufficient plants, DA partially suppresses plant immune response and enhances symbiont colonization without compromising disease resistance.
In Pi‐deficient plants, DA enhances phytohormone‐mediated immune response and causes plant hypersensitivity to Pi deficiency.
A volatile compound produced by a plant growth‐promoting rhizobacterium differentially affects plant immunity and plant response to symbiont colonization depending on phosphate availability.
Effector proteins delivered inside plant cells are powerful weapons for bacterial pathogens, but this exposes the pathogen to potential recognition by the plant immune system. Therefore, the effector ...repertoire of a given pathogen must be balanced for a successful infection. Ralstonia solanacearum is an aggressive pathogen with a large repertoire of secreted effectors. One of these effectors, RipE1, is conserved in most R. solanacearum strains sequenced to date. In this work, we found that RipE1 triggers immunity in N. benthamiana, which requires the immune regulator SGT1, but not EDS1 or NRCs. Interestingly, RipE1-triggered immunity induces the accumulation of salicylic acid (SA) and the overexpression of several genes encoding phenylalanine-ammonia lyases (PALs), suggesting that the unconventional PAL-mediated pathway is responsible for the observed SA biosynthesis. Surprisingly, RipE1 recognition also induces the expression of jasmonic acid (JA)-responsive genes and JA biosynthesis, suggesting that both SA and JA may act cooperatively in response to RipE1. We further found that RipE1 expression leads to the accumulation of glutathione in plant cells, which precedes the activation of immune responses. R. solanacearum secretes another effector, RipAY, which is known to inhibit immune responses by degrading cellular glutathione. Accordingly, RipAY inhibits RipE1-triggered immune responses. This work shows a strategy employed by R. solanacearum to counteract the perception of its effector proteins by plant immune system.
The type-III secreted effector RipE1, from Ralstonia solanacearum, triggers immune responses in Arabidopsis and Nicotiana benthamiana. Such immune responses correlate with an activation of signaling mediated by salicylic acid and jasmonic acid. RipE1-triggered immunity is suppressed by another effector in R. solanacearum, RipAY, showing a bacterial strategy to counteract effector-triggered immunity.
Bacterial wilt caused by the soil-borne plant pathogen Ralstonia solanacearum is a devastating disease worldwide. Upon plant colonization, R. solanacearum replicates massively, causing plant wilting ...and death; collapsed infected tissues then serve as a source of inoculum. In this work, we show that the plant metabolic pathway mediated by pyruvate decarboxylases (PDCs) contributes to plant tolerance to bacterial wilt disease. Arabidopsis and tomato plants respond to R. solanacearum infection by increasing PDC activity, and plants with deficient PDC activity are more susceptible to bacterial wilt. Treatment with either pyruvic acid or acetic acid (substrate and product of the PDC pathway, respectively) enhances plant tolerance to bacterial wilt disease. An effector protein secreted by R. solanacearum, RipAK, interacts with PDCs and inhibits their oligomerization and enzymatic activity. Collectively, our work reveals a metabolic pathway involved in plant resistance to biotic and abiotic stresses, and a bacterial virulence strategy to promote disease and the completion of the pathogenic life cycle.
This study reveals that, upon invasion by Ralstonia solanacearum, bacterial proliferation in plants induces the activation of pyruvate decarboxylases (PDCs), leading to the biosynthesis of acetic acid, which promotes plant tolerance to bacterial wilt. In turn, R. solanacearum secretes a type-III effector that targets PDCs and inhibits their enzymatic activity, promoting the development of disease symptoms.
PDF
