Non-adapted Pathogens Research Articles

Plant resistance to pathogens as a result of gene interaction

Modern information on the genomics of plants and plants’ pathogens as well the achievements of molecular biology have made it possible to state the participation of gene products, proteins, in the organization of molecular complexes that are assembled to implement a certain character of the phenotype. The character of plant “resistance/sensitivity” to a certain biotic factor is also interesting because there is an interaction not only between the genes of one organism, but between the genes of organisms that lie in different kingdoms of life.Plant resistance to pathogens can be passive (provided mainly by characters of plant morphology) and active. Active resistance is formed as a result of the penetration of the pathogen or its elicitors and effectors into the plant. Active protection of the plant at the molecular level is expressed in the launch of the MAPK cascade, the accumulation of reactive oxygen species, and an increase in the flow of calcium ions to the cell. Active protection can be implemented on two levels. The first level, RTI (PAMP Triggered Immunity), develops in response to plant contact with a wide range of non-adapted pathogens. The resistance (immunity) that is formed in this case is called non-specific, or horizontal, or quantitative. The molecular instrument for initiating the defensive reaction is the PRR (Pattern Recognition Receptors). Adapted pathogens are able to overcome RTI by sending effectors to plant cells. These are protein molecules whose function is to create conditions within the cell that are more permissive to the pathogen. The effector can be recognized by the plant’s specific NLR (Nod-Like Receptors), and complementation occurs between the two. There are other specific plant molecules, nonNLR, with a different type of protein product interaction for recognition. In both cases, the second level of protection, ETI (Effector Triggered Immunity), develops. The set of molecular processes that occur at the second level of protection does not differ from the set of the first level, but the processes occur more intensively and are accompanied by the death of the affected cells. This prevents the further spread of the pathogen throughout the plant. The molecular events of the first and second levels of protection are not isolated. The interaction between them involving the products of plant genes and pathogen genes is described by the “zig-zag-zig”-model, invasion model, and the integrated iceberg model. The interaction of plant genes for effector recognition is described by the “guard” and “decoy” models. To initiate a defensive reaction, plant receptors, which can sometimes differentiate into sensors and helpers, form protein complexes, resistosomes.

Light- and Relative Humidity-Regulated Hypersensitive Cell Death and Plant Immunity in Chinese Cabbage Leaves by a Non-adapted Bacteria Xanthomonas campestris pv. vesicatoria.

Inoculation of Chinese cabbage leaves with high titer (107 cfu/ml) of the non-adapted bacteria Xanthomonas campestris pv. vesicatoria (Xcv) strain Bv5-4a.1 triggered rapid leaf tissue collapses and hypersensitive cell death (HCD) at 24 h. Electrolyte leakage and lipid peroxidation markedly increased in the Xcv-inoculated leaves. Defence-related gene expressions (BrPR1, BrPR4, BrChi1, BrGST1 and BrAPX1) were preferentially activated in the Xcv-inoculated leaves. The Xcv-triggered HCD was attenuated by continuous light but accelerated by a dark environment, and the prolonged high relative humidity also alleviated the HCD. Constant dark and increased relative humidity provided favorable conditions for the Xcv bacterial growth in the leaves. Pretreated fluridone (biosynthetic inhibitor of endogenous abscisic acid [ABA]) increased the HCD in the Xcv-inoculated leaves, but exogenous ABA attenuated the HCD. The pretreated ABA also reduced the Xcv bacterial growth in the leaves. These results highlight that the onset of HCD in Chinese cabbage leaves initiated by non-adapted pathogen Xcv Bv5-4a.1 and in planta bacterial growth was differently modulated by internal and external conditional changes.

Vesicle trafficking pathways in defence-related cell wall modifications: papillae and encasements.

Filamentous pathogens that cause plant diseases such as powdery mildew, rust, anthracnose, and late blight continue to represent an enormous challenge for farmers worldwide. Interestingly, these pathogens, although phylogenetically distant, initiate pathogenesis in a very similar way by penetrating the cell wall and establishing a feeding structure inside the plant host cell. To prevent pathogen ingress, the host cell responds by forming defence structures known as papillae and encasements that are thought to mediate pre- and post-invasive immunity, respectively. This form of defence is evolutionarily conserved in land plants and is highly effective and durable against a broad selection of non-adapted filamentous pathogens. As most pathogens have evolved strategies to overcome the defences of only a limited range of host plants, the papilla/encasement response could hold the potential to become an optimal transfer of resistance from one plant species to another. In this review I lay out current knowledge of the involvement of membrane trafficking that forms these important defence structures and highlight some of the questions that still need to be resolved.

Molecular Interplay between Non-Host Resistance, Pathogens and Basal Immunity as a Background for Fatal Yellowing in Oil Palm (Elaeis guineensis Jacq.) Plants.

An oil palm (Elaeis guineensis Jacq.) bud rod disorder of unknown etiology, named Fatal Yellowing (FY) disease, is regarded as one of the top constraints with respect to the growth of the palm oil industry in Brazil. FY etiology has been a challenge embraced by several research groups in plant pathology throughout the last 50 years in Brazil, with no success in completing Koch's postulates. Most recently, the hypothesis of having an abiotic stressor as the initial cause of FY has gained ground, and oxygen deficiency (hypoxia) damaging the root system has become a candidate for stress. Here, a comprehensive, large-scale, single- and multi-omics integration analysis of the metabolome and transcriptome profiles on the leaves of oil palm plants contrasting in terms of FY symptomatology-asymptomatic and symptomatic-and collected in two distinct seasons-dry and rainy-is reported. The changes observed in the physicochemical attributes of the soil and the chemical attributes and metabolome profiles of the leaves did not allow the discrimination of plants which were asymptomatic or symptomatic for this disease, not even in the rainy season, when the soil became waterlogged. However, the multi-omics integration analysis of enzymes and metabolites differentially expressed in asymptomatic and/or symptomatic plants in the rainy season compared to the dry season allowed the identification of the metabolic pathways most affected by the changes in the environment, opening an opportunity for additional characterization of the role of hypoxia in FY symptom intensification. Finally, the initial analysis of a set of 56 proteins/genes differentially expressed in symptomatic plants compared to the asymptomatic ones, independent of the season, has presented pieces of evidence suggesting that breaks in the non-host resistance to non-adapted pathogens and the basal immunity to adapted pathogens, caused by the anaerobic conditions experienced by the plants, might be linked to the onset of this disease. This set of genes might offer the opportunity to develop biomarkers for selecting oil palm plants resistant to this disease and to help pave the way to employing strategies to keep the safety barriers raised and strong.

Nucleotide-binding leucine-rich repeat network underlies nonhost resistance of pepper against the Irish potato famine pathogen Phytophthora infestans.

Nonhost resistance (NHR) is a robust plant immune response against non-adapted pathogens. A number of nucleotide-binding leucine-rich repeat (NLR) proteins that recognize non-adapted pathogens have been identified, although the underlying molecular mechanisms driving robustness of NHR are still unknown. Here, we screened 57 effectors of the potato late blight pathogen Phytophthora infestans in nonhost pepper (Capsicum annuum) to identify avirulence effector candidates. Selected effectors were tested against 436 genome-wide cloned pepper NLRs, and we identified multiple functional NLRs that recognize P. infestans effectors and confer disease resistance in the Nicotiana benthamiana as a surrogate system. The identified NLRs were homologous to known NLRs derived from wild potatoes that recognize P. infestans effectors such as Avr2, Avrblb1, Avrblb2, and Avrvnt1. The identified CaRpi-blb2 is a homologue of Rpi-blb2, recognizes Avrblb2 family effectors, exhibits feature of lineage-specifically evolved gene in microsynteny and phylogenetic analyses, and requires pepper-specific NRC (NLR required for cell death)-type helper NLR for proper function. Moreover, CaRpi-blb2-mediated hypersensitive response and blight resistance were more tolerant to suppression by the PITG_15 278 than those mediated by Rpi-blb2. Combined results indicate that pepper has stacked multiple NLRs recognizing effectors of non-adapted P. infestans, and these NLRs could be more tolerant to pathogen-mediated immune suppression than NLRs derived from the host plants. Our study suggests that NLRs derived from nonhost plants have potential as untapped resources to develop crops with durable resistance against fast-evolving pathogens by stacking the network of nonhost NLRs into susceptible host plants.

Receptor-mediated nonhost resistance in plants.

Nonhost resistance (NHR) is a plant immune response that prevents many microorganisms in the plant’s environment from pathogenicity against the plant. Since successful pathogens have adapted to overcome the immune systems of their host, the durable nature of NHR has potential in the management of plant disease. At present, there is genetic and molecular evidence that the underlying molecular mechanisms of NHR are similar to the plant immune responses that occur in host plants following infection by adapted pathogens. We consider that the molecular basis of NHR is multilayered, conferred by physicochemical barriers and defense responses that are induced following molecular recognition events. Moreover, the relative contribution of each component may depend on evolutionary distances between host and nonhost plants of given pathogen species. This mini-review has focused on the current knowledge of plant NHR, especially the recognition of non-adapted pathogens by nonhost plants at the cellular level. Recent gains in understanding the roles of plasma membrane-localized pattern-recognition receptors (PRRs) and the cytoplasmic nucleotide-binding leucine-rich repeat receptors (NLRs) associated with these processes, as well as the genes involved, are summarized. Finally, we provide a theoretical perspective on the durability of receptor-mediated NHR and its practical potential as an innovative strategy for crop protection against pathogens.

CEP peptide induces susceptibility of Arabidopsis thaliana to non-adapted pathogens

CEP peptide induces susceptibility of Arabidopsis thaliana to non-adapted pathogens

The Pseudomonas syringae type III effector HopG1 triggers necrotic cell death that is attenuated by AtNHR2B

The plant pathogenic bacterium Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) has become a paradigm to investigate plant-bacteria interactions due to its ability to cause disease in the model plant Arabidopsis thaliana. Pst DC3000 uses the type III secretion system to deliver type III secreted effectors (T3SEs) directly into the plant cytoplasm. Pst DC3000 T3SEs contribute to pathogenicity by suppressing plant defense responses and targeting plant’s physiological processes. Although the complete repertoire of effectors encoded in the Pst DC3000 genome have been identified, the specific function for most of them remains to be elucidated. Among those effectors, the mitochondrial-localized T3E HopG1, suppresses plant defense responses and promotes the development of disease symptoms. Here, we show that HopG1 triggers necrotic cell death that enables the growth of adapted and non-adapted pathogens. We further showed that HopG1 interacts with the plant immunity-related protein AtNHR2B and that AtNHR2B attenuates HopG1- virulence functions. These results highlight the importance of HopG1 as a multi-faceted protein and uncover its interplay with AtNHR2B.

Activation of the VQ Motif-Containing Protein Gene VQ28 Compromised Nonhost Resistance of Arabidopsis thaliana to Phytophthora Pathogens.

Nonhost resistance refers to resistance of a plant species to all genetic variants of a non-adapted pathogen. Such resistance has the potential to become broad-spectrum and durable crop disease resistance. We previously employed Arabidopsis thaliana and a forward genetics approach to identify plant mutants susceptible to the nonhost pathogen Phytophthora sojae, which resulted in identification of the T-DNA insertion mutant esp1 (enhanced susceptibility to Phytophthora). In this study, we report the identification of VQ motif-containing protein 28 (VQ28), whose expression was highly up-regulated in the mutant esp1. Stable transgenic A. thaliana plants constitutively overexpressing VQ28 compromised nonhost resistance (NHR) against P. sojae and P. infestans, and supported increased infection of P. parasitica. Transcriptomic analysis showed that overexpression of VQ28 resulted in six differentially expressed genes (DEGs) that are involved in the response to abscisic acid (ABA). High performance liquid chromatography-mass spectrometry (HPLC-MS) detection showed that the contents of endogenous ABA, salicylic acid (SA), and jasmonate (JA) were enriched in VQ28 overexpression lines. These findings suggest that overexpression of VQ28 may lead to an imbalance in plant hormone homeostasis. Furthermore, transient overexpression of VQ28 in Nicotiana benthamiana rendered plants more susceptible to Phytophthora pathogens. Deletion mutant analysis showed that the C-terminus and VQ-motif were essential for plant susceptibility. Taken together, our results suggest that VQ28 negatively regulates plant NHR to Phytophthora pathogens.

Plant SYP12 syntaxins mediate an evolutionarily conserved general immunity to filamentous pathogens.

Filamentous fungal and oomycete plant pathogens that invade by direct penetration through the leaf epidermal cell wall cause devastating plant diseases. Plant preinvasive immunity toward nonadapted filamentous pathogens is highly effective and durable. Pre- and postinvasive immunity correlates with the formation of evolutionarily conserved and cell-autonomous cell wall structures, named papillae and encasements, respectively. Yet, it is still unresolved how papillae/encasements are formed and whether these defense structures prevent pathogen ingress. Here, we show that in Arabidopsis the two closely related members of the SYP12 clade of syntaxins (PEN1 and SYP122) are indispensable for the formation of papillae and encasements. Moreover, loss-of-function mutants were hampered in preinvasive immunity toward a range of phylogenetically distant nonadapted filamentous pathogens, underlining the versatility and efficacy of this defense. Complementation studies using SYP12s from the early diverging land plant, Marchantia polymorpha, showed that the SYP12 clade immunity function has survived 470 million years of independent evolution. These results suggest that ancestral land plants evolved the SYP12 clade to provide a broad and durable preinvasive immunity to facilitate their life on land and pave the way to a better understanding of how adapted pathogens overcome this ubiquitous plant defense strategy.

Preinvasive nonhost resistance of Arabidopsis against melanized appressorium-mediated entry of multiple nonadapted Colletotrichum fungi

ABSTRACT Nonhost plants effectively block a vast number of nonadapted fungal pathogens at the preinvasive stage. On the host plants, adapted fungal pathogens such as Colletotrichum species invade into plant epidermal cell by penetration peg developed from melanized appressorium, followed by invasive hyphal extension. I reported nonadapted Colletotrichum fungi that showed an increased rate of melanized appressorium-mediated entry (MAE) into the pen2 mutant of nonhost Arabidopsis thaliana (hereafter Arabidopsis). It was also found that other MAE-type nonadapted Colletotrichum fungi with no penetration into the pen2 mutant invaded Arabidopsis in the presence of additional mutations such as edr1, gsh1, eds5, cas, and chup1 in the pen2 background. Thus, many immune components contribute to the preinvasive nonhost resistance (NHR) of Arabidopsis against Colletotrichum MAE, and PEN2-related defense takes priority over other defense pathways. Here, I show that among the above nonadapted fungi, Colletotrichum nymphaeae PL1-1-b exhibited relatively lower incompatibility with the nonhost Arabidopsis with increased MAE in each single mutant of edr1, gsh1, eds5, and cas, although other nonadapted fungi almost never invaded these single mutants. Based on the relationships between Colletotrichum MAE and the Arabidopsis immune-related components, Colletotrichum-Arabidopsis incompatibility and multilayered immunity in the preinvasive NHR of Arabidopsis are discussed in this study.

The barley immune receptor Mla recognizes multiple pathogens and contributes to host range dynamics

Crop losses caused by plant pathogens are a primary threat to stable food production. Stripe rust (Puccinia striiformis) is a fungal pathogen of cereal crops that causes significant, persistent yield loss. Stripe rust exhibits host species specificity, with lineages that have adapted to infect wheat and barley. While wheat stripe rust and barley stripe rust are commonly restricted to their corresponding hosts, the genes underlying this host specificity remain unknown. Here, we show that three resistance genes, Rps6, Rps7, and Rps8, contribute to immunity in barley to wheat stripe rust. Rps7 cosegregates with barley powdery mildew resistance at the Mla locus. Using transgenic complementation of different Mla alleles, we confirm allele-specific recognition of wheat stripe rust by Mla. Our results show that major resistance genes contribute to the host species specificity of wheat stripe rust on barley and that a shared genetic architecture underlies resistance to the adapted pathogen barley powdery mildew and non-adapted pathogen wheat stripe rust.

Arabidopsis EXO70B2 exocyst subunit contributes to papillae and encasement formation in antifungal defence.

In the reaction to non-adapted Blumeria graminis f. sp. hordei (Bgh), Arabidopsis thaliana leaf epidermal cells deposit cell wall reinforcements called papillae or seal fungal haustoria in encasements, both of which involve intensive exocytosis. A plant syntaxin, SYP121/PEN1, has been found to be of key importance for the timely formation of papillae, and the vesicle tethering complex exocyst subunit EXO70B2 has been found to contribute to their morphology. Here, we identify a specific role for the EXO70B2-containing exocyst complex in the papillae membrane domains important for callose deposition and GFP-SYP121 delivery to the focal attack sites, as well as its contribution to encasement formation. The mRuby2-EXO70B2 co-localizes with the exocyst core subunit SEC6 and GFP-SYP121 in the membrane domain of papillae, and EXO70B2 and SYP121 proteins have the capacity to directly interact. The exo70B2/syp121 double mutant produces a reduced number of papillae and haustorial encasements in response to Bgh, indicating an additive role of the exocyst in SYP121-coordinated non-host resistance. In summary, we report cooperation between the plant exocyst and a SNARE protein in penetration resistance against non-adapted fungal pathogens.

Arabidopsis CURLY LEAF functions in leaf immunity against fungal pathogens by concomitantly repressing SEPALLATA3 and activating ORA59.

Arabidopsis non-host resistance against non-adapted fungal pathogens including Colletotrichum fungi consists of pre-invasive and post-invasive immune responses. Here we report that non-host resistance against non-adapted Colletotrichum spp. in Arabidopsis leaves requires CURLY LEAF (CLF), which is critical for leaf development, flowering and growth. Microscopic analysis of pathogen behavior revealed a requirement for CLF in both pre- and post-invasive non-host resistance. The loss of a functional SEPALLATA3 (SEP3) gene, ectopically expressed in clf mutant leaves, suppressed not only the defect of the clf plants in growth and leaf development but also a defect in non-host resistance against the non-adapted Colletotrichum tropicale. However, the ectopic overexpression of SEP3 in Arabidopsis wild-type leaves did not disrupt the non-host resistance. The expression of multiple plant defensin (PDF) genes that are involved in non-host resistance against C. tropicale was repressed in clf leaves. Moreover, the Octadecanoid-responsive Arabidopsis 59 (ORA59) gene, which is required for PDF expression, was also repressed in clf leaves. Notably, when SEP3 was overexpressed in the ora59 mutant background, C. tropicale produced clear lesions in the inoculated leaves, indicating an impairment in non-host resistance. Furthermore, ora59 plants overexpressing SEP3 exhibited a defect in leaf immunity to the adapted Colletotrichum higginsianum. Since the ora59 plants overexpressing SEP3 did not display obvious leaf curling or reduced growth, in contrast to the clf mutants, these results strongly suggest that concomitant SEP3 repression and ORA59 induction via CLF are required for Arabidopsis leaf immunity to Colletotrichum fungi, uncoupled from CLF's function in growth and leaf development.

Arabidopsis non-host resistance PSS30 gene enhances broad-spectrum disease resistance in the soybean cultivar Williams 82.

Non-host resistance (NHR), which protects all members of a plant species from non-adapted or non-host plant pathogens, is the most common form of plant immunity. NHR provides the most durable and robust form of broad-spectrum immunity against non-adaptive pathogens pathogenic to other crop species. In a mutant screen for loss of Arabidopsis (Arabidopsis thaliana) NHR against the soybean (Glycine max (L.) Merr.) pathogen Phytophthora sojae, the Phytophthora sojae-susceptible 30 (pss30) mutant was identified. The pss30 mutant is also susceptible to the soybean pathogen Fusarium virguliforme. PSS30 encodes a folate transporter, AtFOLT1, which was previously localized to chloroplasts and implicated in the transport of folate from the cytosol to plastids. We show that two Arabidopsis folate biosynthesis mutants with reduced folate levels exhibit a loss of non-host immunity against P. sojae. As compared to the wild-type Col-0 ecotype, the steady-state folate levels are reduced in the pss1, atfolt1 and two folate biosynthesis mutants, suggesting that folate is required for non-host immunity. Overexpression of AtFOLT1 enhances immunity of transgenic soybean lines against two serious soybean pathogens, the fungal pathogen F. virguliforme and the soybean cyst nematode (SCN) Heterodera glycines. Transgenic lines showing enhanced SCN resistance also showed increased levels of folate accumulation. This study thus suggests that folate contributes to non-host plant immunity and that overexpression of a non-host resistance gene could be a suitable strategy for generating broad-spectrum disease resistance in crop plants.

Arabidopsis nonhost resistance gene PENETRATION 2 is involved in disruption of cushion formation by Rhizoctonia solani during early infection process

Rice sheath blight, a major devastating disease caused by Rhizoctonia solani, poses huge threat to global rice production. Despite being the most hostile necrotrophic fungus with a wide host range, the mechanism involved in R. solani pathobiology is poorly understood. The evolutionarily developed nonhost resistance (NHR) provides broad-spectrum disease resistance to food crops. According to previous reports, Arabidopsis PEN1, PEN2 and PEN3 act as key components of cell wall-based pre-haustorial defenses against non-adapted pathogens. However, the involvement of these PEN genes in NHR against R. solani has remained unexplored till date. Therefore, the objective of this work is to study the efficacy of Arabidopsis PEN genes in NHR against R. solani. For this, hyphal colonization and penetration structures were monitored in Arabidopsis wild type Columbia-0 (Col-0) and mutants- pen1, pen2–3 and pen3–1. Comparatively, R. solani colonization on the leaves of Arabidopsis wild types was less than that on the rice leaf surface. Also, among the pen mutants studied, pen2–3 allowed maximum penetration and colonization by R. solani during early hours of infection as evidenced by both microscopic and macroscopic observations. Advanced lesion area, reduced chlorophyll content and increased fungal biomass accumulation also corroborated with the disease severity in pen2–3. However, R. solani resistance was restored in complemented PEN2-GFP comparable to Col-0. Altogether, our results demonstrate major involvement of PEN2 during pre-penetration, and its contribution to NHR against R. solani for enhanced disease resistance.

The effect of phytoglobin overexpression on the plant proteome during nonhost response of barley (Hordeum vulgare) to wheat powdery mildew (Blumeria graminis f. sp. tritici)

Nonhost resistance, a resistance of plant species against all nonadapted pathogens, is considered the most durable and efficient immune system in plants. To increase our understanding of the response of barley plants to infection by powdery mildew, Blumeria graminis f. sp. tritici, we used quantitative proteomic analysis (LC-MS/MS). We compared the response of two genotypes of barley cultivar Golden Promise, wild type (WT) and plants with overexpression of phytoglobin (previously hemoglobin) class 1 (HO), which has previously been shown to significantly weaken nonhost resistance. A total of 8804 proteins were identified and quantified, out of which the abundance of 1044 proteins changed significantly in at least one of the four comparisons (‘i’ stands for ‘inoculated’)- HO/WT and HOi/WTi (giving genotype differences), and WTi/WT and HOi/HO (giving treatment differences). Among these differentially abundant proteins (DAP) were proteins related to structural organization, disease/defense, metabolism, transporters, signal transduction and protein synthesis. We demonstrate that quantitative changes in the proteome can explain physiological changes observed during the infection process such as progression of the mildew infection in HO plants that was correlated with changes in proteins taking part in papillae formation and preinvasion resistance. Overexpression of phytoglobins led to modification in signal transduction prominently by dramatically reducing the number of kinases induced, but also in the turnover of other signaling molecules such as phytohormones, polyamines and Ca2+. Thus, quantitative proteomics broaden our understanding of the role NO and phytoglobins play in barley during nonhost resistance against powdery mildew.

Moonlighting Function of Phytochelatin Synthase1 in Extracellular Defense against Fungal Pathogens.

Phytochelatin synthase (PCS) is a key component of heavy metal detoxification in plants. PCS catalyzes both the synthesis of the peptide phytochelatin from glutathione and the degradation of glutathione conjugates via peptidase activity. Here, we describe a role for PCS in disease resistance against plant pathogenic fungi. The pen4 mutant, which is allelic to cadmium insensitive1 (cad1/pcs1) mutants, was recovered from a screen for Arabidopsis mutants with reduced resistance to the nonadapted barley fungal pathogen Blumeria graminis f. sp. hordei PCS1, which is found in the cytoplasm of cells of healthy plants, translocates upon pathogen attack and colocalizes with the PEN2 myrosinase on the surface of immobilized mitochondria. pcs1 and pen2 mutant plants exhibit similar metabolic defects in the accumulation of pathogen-inducible indole glucosinolate-derived compounds, suggesting that PEN2 and PCS1 act in the same metabolic pathway. The function of PCS1 in this pathway is independent of phytochelatin synthesis and deglycination of glutathione conjugates, as catalytic-site mutants of PCS1 are still functional in indole glucosinolate metabolism. In uncovering a peptidase-independent function for PCS1, we reveal this enzyme to be a moonlighting protein important for plant responses to both biotic and abiotic stresses.

Non-host resistance of arabidopsis and apple is associated with callose accumulation and changes in preinfective structures of Colletotrichum species

Non-host resistance (NHR) describes the immunity state of plant species against non-adapted pathogen species and has been considered the most durable and effective form of plant resistance in nature. The objective of this work was to study the non-host resistance mechanisms involved in Arabidopsis thaliana and Malus domestica against Colletotrichum fructicola and Colletotrichum higginsianum, respectively. For this, the development of preinfective structures of Colletotrichum species, hypersensitivity responses and callose accumulation were monitored in host and non-host plants. Conidial germination and appressorial formation of Colletotrichum were affected on non-host leaf surfaces. Conidial germination and appressorial melanization of both Colletotrichum species occurred in a faster manner on arabidopsis than on apple leaves. On apple leaves, appressoria of C. higginsianum became more pedicelate, while on its host (arabidopsis) they were typically sessile. Hypersensitive response (HR) and appressorium-associated HR occurred at low frequency in epidermal cells of both plants, and no relationship could be established with NHR. Callose accumulation was significantly higher in inoculated non-host plants, mainly at attempted entry sites of Colletotrichum. Our results demonstrate that the mechanisms of NHR involved in this heterologous interaction were associated to pre-invasive events as demonstrated by the changes in development of preinfective structures and the accumulation of papillary callose at sites of penetration attempts.

Endogenous suppressor(s) in Arabidopsis thaliana

An ethyl acetate extract of Arabidopsis thaliana plants was tested for the presence of endogenous suppressor(s) (ES), and the active fraction, which partitioned into water phase contained a molecule(s) < 3000 Da based on a rough estimate using sized membrane filters. Foliar application of the ES enabled typically nonpathogenic fungi (non-adapted pathogens) to cause disease symptoms on A. thaliana. Consistently, the ES fraction severely suppressed the oxidative burst and the expression of defense-related genes such as FRK1, NHO1, WRKY22, WRKY29, PEN2, and PEN3 in plants challenged with non-adapted fungus Colletotrichum gloeosporioides or the fungal elicitor chitin.