An Arabidopsis callose synthase.

UGT76B1 controls the growth-immunity trade-off during systemic acquired resistance

Accumulation of salicylic acid and PR-1 gene transcripts in relation to the systemic acquired resistance (SAR) response induced by Pseudomonas syringae pv. tomato in Arabidopsis

Plants activate a number of defense reactions in response to pathogen attack. One of the major pathways involves biosynthesis of Salicylic Acid (SA), which acts as a signaling molecule that regulates local defense reaction at the infection site and in induction of systemic acquired resistance (SAR). SA is sensed and transduced by NPR1 protein, which is a redox sensitive protein that acts as a central transcription activator of many pathogenesis related and defense related genes. In its uninduced state NPR1 exists as an oligomer in the cytoplasm. Following pathogen attack and SAR induction, cells undergo a biphasic change in cellular redox, resulting in reduction of NPR1 to a monomeric form,which moves to the nucleus. Recently, it was shown that pathogen attack or SA treatment cause S-nitrosylation of NPR1, promoting NPR1 oligomerization and restricting it in the cytoplasm. We used A. thaliana mutants in cytosolic ASCORBATE PEROXIDASE, apx1, and plants expressing antisense CATALASE gene, as well as the CATALASE inhibitor 3-amino-1,2,4-triazole, to examine the effect of H2O2 on the pathogen-triggered translocation of the NPR1 to the nucleus. Our results show that the pathogen-triggered or SA-induced nuclear translocation is prevented by accumulation of H2O2 in the cytosol. Moreover, we show that increased accumulation of cytoplasmic ROS in apx1 mutants reduced the NPR1-dependent gene expression. We suggest that H2O2 has a signaling role in pathogenesis, acting as a negative regulator of NPR1 translocation to the nucleus, limiting the NPR1-dependent gene expression.

Cells of Pseudomonas phaseolicola were observed entrapped against plant cell walls in both susceptible (Red Kidney) and resistant (Red Mexican) cultivars of French bean (Phaseolus vulgaris). After staining of samples with ruthenium red for electron microscopy pectic polysaccharide within plant cell walls became particularly well contrasted as did fibrillar material connecting bacteria to the plant cell walls. In places this fibrillar material appeared to emanate from the pectic polysaccharide in the plant cell wall, and the plant cell wall surface was eroded at such points. Ruthenium red also stains acidic, bacterial extracellular polysaccharide (EPS) and some of the fibrillar material in intercellular spaces is probably from this source. It is possible that bacteria become attached through an interaction between EPS and Pectic polysaccharide in plant cell walls.

Callose is synthesized on the forming cell plate and several other locations in the plant. We cloned an Arabidopsis cDNA encoding a callose synthase (CalS1) catalytic subunit. The CalS1 gene comprises 42 exons with 41 introns and is transcribed into a 6.0-kb mRNA. The deduced peptide, with an approximate molecular mass of 226 kD, showed sequence homology with the yeast 1,3-beta-glucan synthases and is distinct from plant cellulose synthases. CalS1 contains 16 predicted transmembrane helices with the N-terminal region and a large central loop facing the cytoplasm. CalS1 interacts with two cell plate--associated proteins, phragmoplastin and a novel UDP-glucose transferase that copurifies with the CalS complex. That CalS1 is a cell plate--specific enzyme is demonstrated by the observations that the green fluorescent protein--CalS1 fusion protein was localized at the growing cell plate, that expression of CalS1 in transgenic tobacco cells enhanced callose synthesis on the forming cell plate, and that these cell lines exhibited higher levels of CalS activity. These data also suggest that plant CalS may form a complex with UDP-glucose transferase to facilitate the transfer of substrate for callose synthesis.

NPR1 gene plays an important role in the activation of systemic acquired resistance (SAR). This research was conducted to examine the expression profiles of OsNPR1 gene in four rice varieties: Pongsu Seribu, MR219, MRQ74 and CO39 in response to treatment with salicylic acid (SA). All four varieties vary in their level of resistance to fungal sheath blight disease while Pongsu Seribu showed the highest tolerance. SA treatment did not result in an increase in the level of expression in all varieties except for CO39 which is highly susceptible to blast disease and OsNPR1 expressed in untreated CO39 was lower than the other three varieties. The overall results of this study show that SA did not result in increased expression of OsNPR1 gene in all varieties. We therefore may conclude that exogenous SA does not induce NPR1 gene in rice due to the higher endogenous levels of SA in rice. In addition SAR in rice may be controlled by non SA mediated pathways or combinatorial pathways.Â

Plants being sedentary are subject to invasion by many more pathogens as compared to other mobile eukaryotes. However, these tenacious organisms have developed a vast array of defense mechanisms to ward off invasions. Since constitutive activation of defenses could compromise normal growth, plants have developed complex mechanisms to exert control over these pathways. Plants respond to pathogen invasion by activating the production of antimicrobial compounds, cellwall reinforcement via the synthesis of lignin and callose and by specifically inducing elaborate defense-signaling pathways. The major players regulating the signaling pathways include the plant hormones salicylic acid (SA), jasmonic acid (JA), ethylene (ET) and to a lesser extent, abscisic acid (ABA). Each hormone activates a specific pathway and these act individually, synergistically or antagonistically, depending upon the pathogen involved (see Figure 1 for interactions between the SA, JA and ET pathways). In addition to local resistance, many of these phytohormones also induce defense responses in systemic tissues. Systemic acquired resistance (SAR) is induced in distal tissues following pathogen infection and, conSALICYLIC ACID-, JASMONIC ACIDAND ETHYLENE-MEDIATED REGULATION OF PLANT DEFENSE SIGNALING

To cope with the challenge of pathogens, plants have evolved a wide variety of resistance mechanisms that rely both on constitutive and on inducible defences. Systemic acquired resistance (SAR), a form of inducible resistance that occurs following an earlier localized exposure to a pathogen, provides a long-lasting systemic immunity against a wide range of pathogens in plants. The great benefits of SAR lead to its practical use in agriculture for plant disease management. Pepper (Capsicum annuum) is one of the economically important crops growing worldwide, and in this review, we summarize the scientific research-based studies of SAR in pepper during the past decades. Effects of various exogenous inducers of SAR, such as salicylic acid, DL-β-amino-n-butyric acid, benzothiadiazols and avirulent pathogens on pepper plants have been extensively investigated by different research groups. Biochemical and molecular studies of SAR phenomena also revealed the involvement of radical burst, cell death, endogenous hormonal signalling and defence-related gene expression during SAR establishment in pepper. New knowledge and understanding emerging from the pepper SAR studies will allow the development of novel approaches to enhance the durable resistance of pepper to pathogens, thereby helping to secure the future supply of safe and nutritious pepper worldwide.

Recent advances in systemic acquired resistance research — a review

To clarify the role of ethylene in systemic acquired resistance (SAR), we conducted experiments using Arabidopsis ethylene response mutants. Plants that are nonresponsive to ethylene (i.e., [theta]tr1 and [theta]in2) showed normal sensitivity to the SAR-inducing chemicals salicylic acid (SA) and 2,6-dichloroisonicotinic acid with respect to SAR gene induction and pathogen resistance. This indicated that chemically induced SAR is not an ethylene-dependent process in Arabidopsis. Ethephon, an ethylene-releasing chemical, induced SAR gene expression in both the wild type and ethylene mutants, whereas ethylene alone did not, suggesting that induction of these genes by ethephon is not due to the action of ethylene. Furthermore, transgenic plants expressing salicylate hydroxylase, a bacterial enzyme that degrades SA to catechol, did not accumulate SAR mRNAs in response to ethephon. Thus, SAR gene induction by ethephon appears to be mediated through SA. Other experiments suggested that ethylene may play a role in SAR by enhancing tissue sensitivity to the action of SA.

Systemic acquired resistance (SAR) is a potent innate immunity system in plants that is effective against a broad range of pathogens. SAR in dicotyledonous plants such as tobacco and Arabidopsis has been partially elucidated and is mediated by salicylic acid (SA). However, the SAR mechanism of monocotyledonous rice plants remains to be clarified, although some similarities between SAR mechanisms in both types have been reported. Here we have characterized N-cyanomethyl-2-chloroisonicotinamide (NCI) as an effective SAR inducer in both plant species. Soil drench application of NCI induces a broad range of disease resistance in tobacco and rice and, more specifically, PR gene expression in tobacco. Both SA measurements in wild-type NCI-treated tobacco and pathogenic infection studies using NahG transgenic tobacco plants indicate that NCI-induced resistance enhancement does not require SA. Therefore, it is suggested that NCI induces SAR by triggering signaling at the same level as or downstream of SA accumulation as do both benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester and 2,6-dichloroisonicotinic acid. The fact that all of these chemicals are effective in rice and tobacco suggests that several common components function in disease resistance in both plant species.

BackgroundChitinase, a key enzyme family within the pathogenesis-related (PR) protein, plays a crucial role in plant defense by degrading chitin, a major component of fungal cell walls. The HvCHT genes in barley are involved in responses to biotic and abiotic stresses, although their full range of functions is not yet fully understood.ResultsIn this study, we identified 24 potential HvCHT genes through a genome-wide analysis. The comparative synteny analysis showed conserved relationships between HvCHT genes and their homologs in Sorghum bicolor, Oryza sativa, and Arabidopsis thaliana. Chromosomal mapping, gene structure, characterization, protein motif analysis, and miRNA regulation were performed to gain insight into the genetic structures of these genes. Segmental duplication events observed in the HvCHT family suggest an important role in the evolutionary development of these genes. Additionally, cis-regulatory element analysis revealed the presence of light-responsive elements, and regulators for Abscisic acid, methyl jasmonate (MeJA), salicylic acid, and gibberellins, indicating potential involvement in stress responses. Transcriptomic data showed differential expression of HvCHT genes in response to salt stress, with distinct patterns observed in leaf and root tissues. Furthermore, the genes defensive responses to drought stress and Fusarium infection were characterized across multiple time points. Notably, qRT-PCR analysis confirmed the upregulation of HvCHT1, HvCHT4, and HvCHT17, highlighting their potential involvement in stress-related pathways.ConclusionThese findings provide a comprehensive overview of the HvCHT genes role in barley defense mechanisms, underlining their regulatory functions in biotic and abiotic stressors. The results lay the groundwork for future functional studies on HvCHT genes, with the potential to enhance stress tolerance in crops.Clinical trial numberNot applicable.

Botrytis cinerea is a non-specific necrotrophic pathogen that attacks more than 200 plant species. In contrast to biotrophs, the necrotrophs obtain their nutrients by first killing the host cells. Many studies have shown that infection of plants by necrosis-causing pathogens induces a systemic acquired resistance (SAR), which provides protection against successive infections by a range of pathogenic organisms. We analyzed the role of SAR in B. cinerea infection of Arabidopsis. We show that although B. cinerea induced necrotic lesions and camalexin biosynthesis, it did not induce SAR-mediated protection against virulent strains of Pseudomonas syringae, or against subsequent B. cinerea infections. Induction of SAR with avirulent P. syringae or by chemical treatment with salicylic acid (SA) or benzothiadiazole also failed to inhibit B. cinerea growth, although removal of basal SA accumulation by expression of a bacterial salicylate hydroxylase (NahG) gene or by infiltration of 2-aminoindan-2-phosphonic acid, an inhibitor of phenylpropanoid pathway, increased B. cinerea disease symptoms. In addition, we show that B. cinerea induced expression of genes associated with SAR, general stress and ethylene/jasmonate-mediated defense pathways. Thus, B. cinerea does not induce SAR nor is it affected by SAR, making it a rare example of a necrogenic pathogen that does not cause SAR.

Soybean plant is characterized by a systemic autoregulatory control system of nodulation (autoregulation) by initial infection with rhizobia, and plants commonly display a systemic acquired resistance (SAR) to pathogenic microbe infection related to salicylic acid (SA) signal transmission. We investigated the effect of exogenous SA supply on soybean nodulation to determine whether SA affects the autoregulation of nodulation. Seedlings of the hypernodulating mutants NOD1-3, NOD2-4 and their parent cv. Williams were treated or not treated (control) with a 100 μmS-SA solution at 5 d before the inoculation of Bradyrhizobium japonicum strain USDA110. The nodule dry weight and the number of nodules of the wild type soybean Williams exhibiting autoregulation drastically decreased by the addition of 100 μm SA. The decrease in the nodule number was not caused by the reduction of the rhizobium number in the medium. Salicylic acid inhibited only early nodule formation and did not affect the growth of formed nodules. The inhibitory effect of SA on the nodulation of NOD1-3 and NOD2-4 was significantly less pronounced than that in Williams. These results indicate that SA is directly involved in signal transmission in the autoregulation, and that SA or the SAR induced by SA stimulates the autoregulation of nodulation in soybean.

The plant hormone salicylic acid (SA) is essential for local defense and systemic acquired resistance (SAR). When plants, such as Arabidopsis, are challenged by different pathogens, an increase in SA biosynthesis generally occurs through transcriptional induction of the key synthetic enzyme isochorismate synthase 1 (ICS1). However, the regulatory mechanism for this induction is poorly understood. Using a yeast one-hybrid screen, we identified two transcription factors (TFs), NTM1-like 9 (NTL9) and CCA1 hiking expedition (CHE), as activators of ICS1 during specific immune responses. NTL9 is essential for inducing ICS1 and two other SA synthesis-related genes, phytoalexin-deficient 4 (PAD4) and enhanced disease susceptibility 1 (EDS1), in guard cells that form stomata. Stomata can quickly close upon challenge to block pathogen entry. This stomatal immunity requires ICS1 and the SA signaling pathway. In the ntl9 mutant, this response is defective and can be rescued by exogenous application of SA, indicating that NTL9-mediated SA synthesis is essential for stomatal immunity. CHE, the second identified TF, is a central circadian clock oscillator and is required not only for the daily oscillation in SA levels but also for the pathogen-induced SA synthesis in systemic tissues during SAR. CHE may also regulate ICS1 through the known transcription activators calmodulin binding protein 60g (CBP60g) and systemic acquired resistance deficient 1 (SARD1) because induction of these TF genes is compromised in the che-2 mutant. Our study shows that SA biosynthesis is regulated by multiple TFs in a spatial and temporal manner and therefore fills a gap in the signal transduction pathway between pathogen recognition and SA production.