PSKR1 and PSY1R-mediated regulation of plant defense responses

Plant peptide signaling is an upcoming topic in many areas of plant research. Our recent findings show that the tyrosine sulfated peptide receptors PSKR1 and PSY1R are not only involved in growth and development but also in plant defense. They modulate salicylate- and jasmonate-dependent defense pathways in an antagonistic manner and this phenomenon might be dependent on the age and developmental stage of the plant. Here we discuss how the endogenous peptides might integrate growth, wounding, senescence and the opposing defense pathways against biotrophic and necrotrophic pathogens for increased fitness of the plant.     

一氧化氮与激发子诱导的植物抗病防卫反应

来源于真菌或植物细胞壁的激发子可以诱导植物的抗性反应。一系列的信号分子,如一氧化氮、活性氧、茉莉酸、水杨酸、乙烯等都参与了激发子诱导的植物抗性反应。它们在介导激发子刺激诱发胞内抗性反应的过程中起着重要的作用。本文介绍了激发子的种类,并简述了激发了受体以及植物细胞对激发子刺激的感受与传递;重点介绍了一氧化氮在激发子诱导植物抗性反应过程中的作用,以及它与其他信号分子之间相互关系的研究进展。     

Elicitors and priming agents initiate plant defense responses

Biotic elicitors produced by plant pathogens or herbivore pests rapidly activate a range of plant chemical defenses when translocated to plant tissue. The fatty acid conjugate volicitin has proven to be a robust elicitor model for studying herbivore-induced plant defense responses. Here we review the role of insect-derived volicitin (N-[17-hydroxylinolenoyl]-L-glutamine) as an authentic elicitor of defense responses, specifically as an activator of signal volatiles that attract natural enemies of herbivore pests. Comparisons are drawn between volicitin as an elicitor of plant defenses and two other classes of signaling molecules, C₆ green-leaf volatiles and C₄ bacterial volatiles that appear to prime plant defenses thereby enhancing the capacity to mobilize cellular defense responses when a plant is faced with herbivore or pathogen attack.     

Nanosecond electric pulses trigger actin responses in plant cells

We have analyzed the cellular effects of nanosecond pulsed electrical fields on plant cells using fluorescently tagged marker lines in the tobacco cell line BY-2 and confocal laser scanning microscopy. We observe a disintegration of the cytoskeleton in the cell cortex, followed by contraction of actin filaments towards the nucleus, and disintegration of the nuclear envelope. These responses are accompanied by irreversible permeabilization of the plasma membrane manifest as uptake of Trypan Blue. By pretreatment with the actin-stabilizing drug phalloidin, the detachment of transvacuolar actin from the cell periphery can be suppressed, and this treatment can also suppress the irreversible perforation of the plasma membrane. We discuss these findings in terms of a model, where nanosecond pulsed electric fields trigger actin responses that are key events in the plant-specific form of programmed cell death.     

Erwinia amylovora type three-secreted proteins trigger cell death and defense responses in Arabidopsis thaliana

Erwinia amylovora is the bacterium responsible for fire blight, a necrotic disease affecting plants of the rosaceous family. E. amylovora pathogenicity requires a functional type three secretion system (T3SS). We show here that E. amylovora triggers a T3SS-dependent cell death on Arabidopsis thaliana. The plants respond by inducing T3SS-dependent defense responses, including salicylic acid (SA)-independent callose deposition, activation of the SA defense pathway, reactive oxygen species (ROS) accumulation, and part of the jasmonic acid/ethylene defense pathway. Several of these reactions are similar to what is observed in host plants. We show that the cell death triggered by E. amylovora on A. thaliana could not be simply explained by the recognition of AvrRpt2 ea by the resistance gene product RPS2. We then analyzed the role of type three-secreted proteins (T3SPs) DspA/E, HrpN, and HrpW in the induction of cell death and defense reactions in A. thaliana following infection with the corresponding E. amylovora mutant strains. HrpN and DspA/E were found to play an important role in the induction of cell death, activation of defense pathways, and ROS accumulation. None of the T3SPs tested played a major role in the induction of SA-independent callose deposition. The relative importance of T3SPs in A. thaliana is correlated with their relative importance in the disease process on host plants, indicating that A. thaliana can be used as a model to study their role.     

Nonpathogenic strains of Colletotrichum lindemuthianum trigger progressive bean defense responses during appressorium-mediated penetration

The fungal bean pathogen Colletotrichum lindemuthianum differentiates appressoria in order to penetrate bean tissues. We showed that appressorium development in C. lindemuthianum can be divided into three stages, and we obtained three nonpathogenic strains, including one strain blocked at each developmental stage. H18 was blocked at the appressorium differentiation stage; i.e., no genuine appressoria were formed. H191 was blocked at the appressorium maturation stage; i.e., appressoria exhibited a pigmentation defect and developed only partial internal turgor pressure. H290 was impaired in appressorium function; i.e., appressoria failed to penetrate into bean tissues. Furthermore, these strains could be further discriminated according to the bean defense responses that they induced. Surprisingly, appressorium maturation, but not appressorium function, was sufficient to induce most plant defense responses tested (superoxide ion production and strong induction of pathogenesis-related proteins). However, appressorium function (i.e., entry into the first host cell) was necessary for avirulence-mediated recognition of the fungus.     

A pilot plant for detoxification of aflatoxin B1-contaminated coconut oil by solar irradiation

Summary In coconut oil naturally contaminated with aflatoxin B1, more than 85% of the toxin is present in the soluble form, the remainder occuring in the sediment. This aflatoxin is detoxified when the oil, in a static layer less than 15 mm thick is exposed to solar radiation. A pilot plant, designed to take account of the viscosity and flow characteristics of the oil, was constructed for the exposure of thin layers of oil (2 mm or less) flowing under gravity. At aflatoxin concentrations between 166 and 1250 jug/kg, 75% of the toxin was degraded on exposure to solar radiation of 10 cal/cm²; total detoxification was achieved on repeated exposure. The naturally contaminated coconut oil after exposure to solar radiation did not contain any residual aflatoxins or fluorescent compounds which might have been derived from original aflatoxin B1.

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Resumen Planta pilota para el tratramiento de aceite de coco contaminado con aflatoxina B1 mediante radiation solar y centrifugado En aceite de coco contaminado de forma natural con aflatoxina B1, más del 85% de la toxina se encuentra en forma soluble, el resto permaneciendo en el sedimento. Esta aflatoxina pierde sus propiedades tóxicas cuando se expone el aceite en forma de capa estática de 15 mm de grosor a la radiación solar. Se construyó una planta piloto diseñada teniendo en cuenta la viscosidad y las caracteristicas de fluidez del aceite de forma que pudieran exponerse a la radiación solar capas de aceite muy finas (2 mm o menos) fluyendo gracias a la gravedad. Cuando aceite conteniendo aflatoxina en proporciones entre 166 y 1250 /kg se expuso a una radiación solar de 10 cal./cm² la toxina se degradó en un 75%. La detoxificación total se obtuvo mediante repetición del proceso. El aceite de coco contaminado de forma natural, una vez expuesto a la radiación solar no contenía aflatoxinas residuales ni compuestos fluorescentes potencialmente derivados de la aflatoxina B1 contenida originalmente.

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Résumé Usine-pilote pour la détoxification, par irradiation solaire et centrifugation, de l'huile de coprah contaminée par l'aflatoxine B1 Dans l'huile de coprah spontanément contaminée par l'aflatoxine B1, plus de 85% de la toxine est présente sous forme soluble, le reste se trouvant dans le sédiment. Cette aflatoxine est détoxifiée lorsque l'huile est exposée à la radiation solaire en couche statique de moins de 15 mm d'épaisseur. Une usine-pilote, conçue en tenant compte de la viscosité et de l'écoulement de l'huile, a été construite pour irradier une mince couche d'huile (2 mm ou moins) s'écoulant par gravité. Pour des concentrations en aflatoxine allant de 166 à 1250 g/kg, 75% de la toxine est dégradée par exposition à une irradiation solaire de 10 cal./cm² et, en répétant le traitement, on obtient une détoxification complète. Après exposition à la radiation solaire, l'huile de coprah contaminée spontanément ne contient plus d'aflatoxine résiduelle, ni de composés fluorescents dérivés de l'aflatoxine B1 originelle.

     

Herbivore-specific plant volatiles prime neighboring plants for nonspecific defense responses

Plants produce species-specific herbivore-induced plant volatiles (HIPVs) after damage. We tested the hypothesis that herbivore-specific HIPVs prime neighboring plants to induce defenses specific to the priming herbivore. Since Manduca sexta (specialist) and Heliothis virescens (generalist) herbivory induced unique HIPV profiles in Nicotiana benthamiana, we used these HIPVs to prime receiver plants for defense responses to simulated herbivory (mechanical wounding and herbivore regurgitant application). Jasmonic acid (JA) accumulations and emitted volatile profiles were monitored as representative defense responses since JA is the major plant hormone involved in wound and defense signaling and HIPVs have been implicated as signals in tritrophic interactions. Herbivore species-specific HIPVs primed neighboring plants, which produced 2 to 4 times more volatiles and JA after simulated herbivory when compared to similarly treated constitutive volatile-exposed plants. However, HIPV-exposed plants accumulated similar amounts of volatiles and JA independent of the combination of priming or challenging herbivore. Furthermore, volatile profiles emitted by primed plants depended only on the challenging herbivore species but not on the species-specific HIPV profile of damaged emitter plants. This suggests that feeding by either herbivore species primed neighboring plants for increased HIPV emissions specific to the subsequently attacking herbivore and is probably controlled by JA.     

Small GTPase 'Rop': molecular switch for plant defense responses

The conserved Rho family of GTPases (Rho, Rac, and Cdc42) in fungi and mammals has emerged as a key regulator of diverse cellular activities, such as cytoskeletal rearrangements, programmed cell death, stress-induced signaling, and cell growth and differentiation. In plants, a unique class of Rho-like proteins, most closely related to mammalian Rac, has only been found and termed 'Rop' (Rho-related GTPase from plant [Li et al. (1998) Plant Physiol. 118, 407-417; Yang (2002) Plant Cell 14, S375-S388]). ROPs have been implicated in regulating various plant cellular responses including defense against pathogens. It has been shown that ROPs, like mammalian Rac, trigger hydrogen peroxide production and hence the 'oxidative burst', a crucial component associated with the cell death, most likely via activation of nicotinamide adenine dinucleotide phosphate oxidase in both monocotyledonous and dicotyledonous species. Recent studies have established that ROPs also function as a molecular switch for defense signaling pathway(s) linked with disease resistance. As discerning the defense pathway remains one of the priority research areas in the field of plant biology, this review is therefore particularly focused on recent progresses that have been made towards understanding the plant defense responses mediated by ROPs.     

Regulatory mechanisms of host plant defense responses to arbuscular mycorrhiza

Arbuscular mycorrhizal (AM) fungi colonize the roots of over 80% of terrestrial plant species, forming mutually beneficial symbioses. During the colonization process, symbiotic partners recognize each other, and undergo observable morphological and physiological changes; indicating that symbiosis formation involves multiple factors that are finely regulated. Sometimes host plants generate a transient, weak, defense response. This response and its down-regulation play a very important role in the development of AM symbioses. Although AM fungi can infect a wide range of host root tissues, which host defense may play a crucial role is hypothesized from the fact that hyphal expansion is only observed in the root cortex.
We discuss five defense mechanisms. (1) The degradation of exogenous elicitors. The host’s weak defense response may be due to the degradation of the exogenous elicitor chitin, or the prevention of release of an endogenous inductor from the plant cell wall. (2) The inactivation of defense signal molecules. Some defense signal molecules such as hydrogen peroxidase, salicylic acid (SA), and jasmonic acid (JA), are inactivated in host plants. This helps to avoid the turn-on of defense-related genes and facilitate mycorrhizal formation. (3) The regulation of plant hormones and plant photosynthates. Plant hormone levels and plant photosynthate metabolism both change during AM colonization. These mechanisms need further exploration. (4) Changes in levels of phosphorous (P), and (iso)flavonoids. High P levels can induce some defense genes to express hydrogen peroxidase, chitinase, and glucanase. These gene products can repress colonization by AM fungi. The plant defense response regulatory effect for different (iso)flavonoids varies, and their levels are regulated by P. (5) The suppressed expression of symbiotic genes. Some symbiosis-related genes inhibit plant defense responses, but it is still unclear which mechanisms underlie gene regulation. We provide here a theoretical basis for research into AM symbiosis that may promote study of host plant resistance and the mechanisms of symbiosis formation.
We provide a deeper insight into the signal transduction pathways of mycorrhization that will aid understanding and analysis of plant defense mechanisms in the AM context. The on-going development of genome sequencing technology will contribute greatly to the detailed study of symbiosis-related genes, and pathogenesis-related protein genes. These related genes may be induced to express corresponding proteins, be repressed, postpone expression or even shutdown, or both may work together to form symbioses. Elucidation of these features will help us understand the roles that plant defenses play in mycorrhizal formation; providing an unprecedented opportunity for research into mycorrhizal molecular biology and the interaction of symbiotic partners, and allowing the underlying mechanisms to be gradually uncovered.     

Regulatory mechanisms of host plant defense responses to arbuscular mycorrhiza

Arbuscular mycorrhizal (AM) fungi colonize the roots of over 80% of terrestrial plant species, forming mutually beneficial symbioses. During the colonization process, symbiotic partners recognize each other, and undergo observable morphological and physiological changes; indicating that symbiosis formation involves multiple factors that are finely regulated. Sometimes host plants generate a transient, weak, defense response. This response and its down-regulation play a very important role in the development of AM symbioses. Although AM fungi can infect a wide range of host root tissues, which host defense may play a crucial role is hypothesized from the fact that hyphal expansion is only observed in the root cortex.
We discuss five defense mechanisms. (1) The degradation of exogenous elicitors. The host’s weak defense response may be due to the degradation of the exogenous elicitor chitin, or the prevention of release of an endogenous inductor from the plant cell wall. (2) The inactivation of defense signal molecules. Some defense signal molecules such as hydrogen peroxidase, salicylic acid (SA), and jasmonic acid (JA), are inactivated in host plants. This helps to avoid the turn-on of defense-related genes and facilitate mycorrhizal formation. (3) The regulation of plant hormones and plant photosynthates. Plant hormone levels and plant photosynthate metabolism both change during AM colonization. These mechanisms need further exploration. (4) Changes in levels of phosphorous (P), and (iso)flavonoids. High P levels can induce some defense genes to express hydrogen peroxidase, chitinase, and glucanase. These gene products can repress colonization by AM fungi. The plant defense response regulatory effect for different (iso)flavonoids varies, and their levels are regulated by P. (5) The suppressed expression of symbiotic genes. Some symbiosis-related genes inhibit plant defense responses, but it is still unclear which mechanisms underlie gene regulation. We provide here a theoretical basis for research into AM symbiosis that may promote study of host plant resistance and the mechanisms of symbiosis formation.
We provide a deeper insight into the signal transduction pathways of mycorrhization that will aid understanding and analysis of plant defense mechanisms in the AM context. The on-going development of genome sequencing technology will contribute greatly to the detailed study of symbiosis-related genes, and pathogenesis-related protein genes. These related genes may be induced to express corresponding proteins, be repressed, postpone expression or even shutdown, or both may work together to form symbioses. Elucidation of these features will help us understand the roles that plant defenses play in mycorrhizal formation; providing an unprecedented opportunity for research into mycorrhizal molecular biology and the interaction of symbiotic partners, and allowing the underlying mechanisms to be gradually uncovered.     

Preliminary studies on differential defense responses induced during plant communication

We compared the expression patterns of three representative genes in undamaged tomato and tobacco plants in response to exposure to either tomato or tobacco fed on by Helicoverpa armigera (cotton bollworm). When tomato and tobacco, two species of one family, were incubated in the chambers with the tomato plants damaged by the cotton bollworm, the expression of the PR1, BGL2, and PAL genes was up-regulated in leaves of both plants. However, the levels of gene expression were significantly higher in the tomato than that in the tobacco. In addition, the activities of enzymes, peroxidase, polyphenol oxidase, and lipoxygenase were found to be higher in the tomato than those in the tobacco. Similar results were obtained when the damaged plants were replaced by the tobacco.     

The Arabidopsis glucosyltransferase UGT76B1 conjugates isoleucic acid and modulates plant defense and senescence

Plants coordinate and tightly regulate pathogen defense by the mostly antagonistic salicylate (SA)- and jasmonate (JA)-mediated signaling pathways. Here, we show that the previously uncharacterized glucosyltransferase UGT76B1 is a novel player in this SA-JA signaling crosstalk. UGT76B1 was selected as the top stress-induced isoform among all 122 members of the Arabidopsis thaliana UGT family. Loss of UGT76B1 function leads to enhanced resistance to the biotrophic pathogen Pseudomonas syringae and accelerated senescence but increased susceptibility toward necrotrophic Alternaria brassicicola. This is accompanied by constitutively elevated SA levels and SA-related marker gene expression, whereas JA-dependent markers are repressed. Conversely, UGT76B1 overexpression has the opposite effect. Thus, UGT76B1 attenuates SA-dependent plant defense in the absence of infection, promotes the JA response, and delays senescence. The ugt76b1 phenotypes were SA dependent, whereas UGT76B1 overexpression indicated that this gene possibly also has a direct effect on the JA pathway. Nontargeted metabolomic analysis of UGT76B1 knockout and overexpression lines using ultra-high-resolution mass spectrometry and activity assays with the recombinant enzyme led to the ab initio identification of isoleucic acid (2-hydroxy-3-methyl-pentanoic acid) as a substrate of UGT76B1. Exogenously applied isoleucic acid increased resistance against P. syringae infection. These findings indicate a novel link between amino acid-related molecules and plant defense that is mediated by small-molecule glucosylation.