Induction Of Systemic Acquired Resistance Research Articles

Long distance movement of DIR1 and investigation of the role of DIR1-like during systemic acquired resistance in Arabidopsis

DIR1 is a lipid transfer protein (LTP) postulated to complex with and/or chaperone a signal(s) to distant leaves during Systemic Acquired Resistance (SAR) in Arabidopsis. DIR1 was detected in phloem sap-enriched petiole exudates collected from wild-type leaves induced for SAR, suggesting that DIR1 gains access to the phloem for movement from the induced leaf. Occasionally the defective in induced resistance1 (dir1-1) mutant displayed a partially SAR-competent phenotype and a DIR1-sized band in protein gel blots was detected in dir1-1 exudates suggesting that a highly similar protein, DIR1-like (At5g48490), may contribute to SAR. Recombinant protein studies demonstrated that DIR1 polyclonal antibodies recognize DIR1 and DIR1-like. Homology modeling of DIR1-like using the DIR1-phospholipid crystal structure as template, provides clues as to why the dir1-1 mutant is rarely SAR-competent. The contribution of DIR1 and DIR1-like during SAR was examined using an Agrobacterium-mediated transient expression-SAR assay and an estrogen-inducible DIR1-EGFP/dir1-1 line. We provide evidence that upon SAR induction, DIR1 moves down the leaf petiole to distant leaves. Our data also suggests that DIR1-like displays a reduced capacity to move to distant leaves during SAR and this may explain why dir1-1 is occasionally SAR-competent.

Induction of Systemic Acquired Resistance by Heat Shock Treatment inArabidopsis

Systemic acquired resistance (SAR) is a potent innate immunity system in plants and has been used in rice fields. Development of SAR, involving priming, is achieved by activation of salicylic acid (SA)-mediated pathway. To determine whether heat shock (HS) treatment can induce SAR, we analyzed the effects of HS on Arabidopsis. HS treatment induced disease resistance, expression of SAR marker genes, and SA accumulation in wild-type but not in SA-deficient sid2 and NahG plants, indicating induction of SAR. Time course analysis of the effects of HS indicated that SAR was activated transiently, differently from biological induction, with a peak at 2-3 d after HS, and that it ceased in several days. Production of reactive oxygen species was observed before SA biosynthesis, which might be a trigger for SAR activation. The data presented here suggest that HS can induce SAR, but there exist unknown regulation mechanisms for the maintenance of SAR.

Efficacy of systemic acquired resistance inducers in olive leaf spot management

Olive leaf spot caused by Spilocaea oleagina is mainly controlled by copper fungicides but there is a growing need for alternative control strategies, such as induced resistance. This study investigated the potential for control of the disease with products reported to induce systemic acquired resistance. The eight products: salicylic acid (SA), 5‐chlorosalicylic acid, chitosan, brotomax, 3-amino butyric acid, Foli-R-Fos 400, acibenzolar-S-methyl, potassium silicate and copper sulphate fungicide were used as foliar spray applications, and potassium silicate also as a soil drench. All compounds except brotomax, 5-chlorosalicylic acid and potassium silicate (foliar spray) reduced disease severity, by 48–89 %, with salicylic acid being most effective. SA reduced disease severity by 89 and 87 % when applied 2 or 4 weeks prior to inoculation, respectively, which was similar to the standard copper sulphate spray. In general, the inducers were more effective in reducing disease severity when plants were treated twice than when treated once prior to inoculation. The level of disease reduction was similar for all treatments (68–86 %) when applied 4 + 2 weeks prior to pathogen inoculation, except for brotomax (52 %). This investigation has identified products that may be used in organic or integrated management programmes for control of olive leaf spot, thereby reducing potential harmful effects such as fungicide resistance and accumulation of copper in orchard soils.

Efficacy of Acibenzolar‐S‐Methyl and β‐Aminobutyric Acid for Control of Downy Mildew in Greenhouse Grown Basil and Peroxidase Activity in Response to Treatment with these Compounds

AbstractDowny mildew, caused by the oomycete pathogen Peronospora belbahrii, is a devastating foliar disease of basil in the United States and worldwide. Currently there are very few chemistries or organic choices registered to control this disease. In this study, two systemic acquired resistance (SAR) inducers, acibenzolar‐S‐methyl (ASM) and β‐aminobutyric acid (BABA), were evaluated for their in vitro effects on the pathogen, for their potential to control basil downy mildew in greenhouses, and for changes in peroxidase activity in basil plants treated with these two SAR inducers. No significant inhibition of sporangial germination was detected in water agar amended with ASM at concentrations lower than 100 mg/l or with BABA at concentrations lower than 500 mg/l. Efficacy of ASM and BABA in greenhouses varied depending on the rate, method and timing of application. The area under the disease progress curve (AUDPC) of disease severity was significantly reduced compared to the non‐treated control when ASM was sprayed (in all experiments) or drenched (in one out of two experiments) pre‐, or pre‐ + post‐inoculation at rates of 25–400 mg/l. Three weekly post‐inoculation sprays of ASM at the rate of 50 mg/l reduced AUDPC by 93.0 and 47.2% when started 3 and 7 days after inoculation (DAI), respectively. The AUDPC of disease severity was also significantly reduced when BABA was sprayed pre‐ + post‐inoculation at rates of 125–500 mg/l. According to the prediction using a log‐logistic function, 50% maximum disease protection was achieved at a concentration of 27.5 mg/l of ASM. Basil plants treated with these two SAR inducers and challenged with the pathogen showed significantly higher peroxidase activity than the non‐treated control at 8 DAI. Temporally, the highest activity of peroxidase was detected at 8 DAI, decreased at 15 DAI and waned further at 23 DAI.

The Arabidopsis mediator complex subunit16 positively regulates salicylate-mediated systemic acquired resistance and jasmonate/ethylene-induced defense pathways.

Systemic acquired resistance (SAR) is a long-lasting plant immunity against a broad spectrum of pathogens. Biological induction of SAR requires the signal molecule salicylic acid (SA) and involves profound transcriptional changes that are largely controlled by the transcription coactivator nonexpressor of pathogenesis-related genes1 (NPR1). However, it is unclear how SAR signals are transduced from the NPR1 signaling node to the general transcription machinery. Here, we report that the Arabidopsis thaliana Mediator subunit16 (MED16) is an essential positive regulator of SAR. Mutations in MED16 reduced NPR1 protein levels and completely compromised biological induction of SAR. These mutations also significantly suppressed SA-induced defense responses, altered the transcriptional changes induced by the avirulent bacterial pathogen Pseudomonas syringae pv tomato (Pst) DC3000/avrRpt2, and rendered plants susceptible to both Pst DC3000/avrRpt2 and Pst DC3000. In addition, mutations in MED16 blocked the induction of several jasmonic acid (JA)/ethylene (ET)-responsive genes and compromised resistance to the necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola. The Mediator complex acts as a bridge between specific transcriptional activators and the RNA polymerase II transcription machinery; therefore, our data suggest that MED16 may be a signaling component in the gap between the NPR1 signaling node and the general transcription machinery and may relay signals from both the SA and the JA/ET pathways.

Expression of the Human NAD(P)-Metabolizing Ectoenzyme CD38 Compromises Systemic Acquired Resistance inArabidopsis

Plant systemic acquired resistance (SAR) is a long-lasting, broad-spectrum immune response that is mounted after primary pathogen infection. Although SAR has been extensively researched, the molecular mechanisms underlying its activation have not been completely understood. We have previously shown that the electron carrier NAD(P) leaks into the plant extracellular compartment upon pathogen attack and that exogenous NAD(P) activates defense gene expression and disease resistance in local treated leaves, suggesting that extracellular NAD(P) [eNAD(P)] might function as a signal molecule activating plant immune responses. To further establish the function of eNAD(P) in plant immunity, we tested the effect of exogenous NAD(P) on resistance gene-mediated hypersensitive response (HR) and SAR. We found that exogenous NAD(P) completely suppresses HR-mediated cell death but does not affect HR-mediated disease resistance. Local application of exogenous NAD(P) is unable to induce SAR in distal tissues, indicating that eNAD(P) is not a sufficient signal for SAR activation. Using transgenic Arabidopsis plants expressing the human NAD(P)-metabolizing ectoenzyme CD38, we demonstrated that altering eNAD(P) concentration or signaling compromises biological induction of SAR. This result suggests that eNAD(P) may play a critical signaling role in activation of SAR.

Evaluation of systemic acquired resistance inducers for control of downy mildew on basil

Basil downy mildew, caused by Peronospora belbahrii Thines sp. nov., is a devastating foliar disease of fresh-cut basil first discovered in the U.S. in South Florida in 2007. Since then the pathogen has been found in over 20 U.S. states and has become a major threat to sweet basil production. In this study, acibenzolar-S-methyl (ASM, Actigard 50WG), DL-3-aminobutyric acid (BABA), isonicotinic acid (INA), salicylic acid (SA) and sodium salicylate (SS) were evaluated for their potential to control basil downy mildew in the greenhouse. Efficacy of these systemic acquired resistance (SAR) inducers varied in control of basil downy mildew depending on the rate, method and timing of application. Foliar sprays of ASM applied pre-, post- or pre- + post-inoculation at rates ranging from 25 to 400 mg l−1 significantly (P = 0.05) reduced disease severity compared to the non-treated control in all experiments. ASM sprayed at 50 mg l−1 three times on a weekly basis starting 3 and 7 days post- inoculation resulted in a 93.8 and 47.1% reduction in disease severity, respectively. Six weekly foliar sprays of BABA as pre- + post-inoculation at rates equal or higher than 125 mg l−1 significantly suppressed downy mildew compared to the non-treated control. Foliar treatments of ASM or BABA followed by one or two post-inoculation sprays of a mixture of potassium phosphite (Prophyt) and azoxystrobin (Quadris) significantly improved efficacy for disease control. Sporangia counted on ASM treated leaves were significantly lower than leaves sampled from the non-treated control. ASM and BABA at concentrations lower than 1.0 mM did not inhibit sporangial germination in vitro. The effect of INA, SA and SS on disease reduction was generally inconsistent and not significant compared to the non-treated control.

An abietane diterpenoid is a potent activator of systemic acquired resistance

Abietane diterpenoids are major constituents of conifer resins that have important industrial and medicinal applications. However, their function in plants is poorly understood. Here we show that dehydroabietinal (DA), an abietane diterpenoid, is an activator of systemic acquired resistance (SAR), which is an inducible defense mechanism that is activated in the distal, non-colonized, organs of a plant that has experienced a local foliar infection. DA was purified as a SAR-activating factor from vascular sap of Arabidopsis thaliana leaves treated with a SAR-inducing microbe. Locally applied DA is translocated through the plant and systemically induces the accumulation of salicylic acid (SA), an important activator of defense, thus leading to enhanced resistance against subsequent infections. The NPR1 (NON-EXPRESSOR OF PR GENES1), FMO1 (FLAVIN-DEPENDENT MONOOXYGENASE1) and DIR1 (DEFECTIVE IN INDUCED RESISTANCE1) genes, which are critical for biologically induced SAR, are also required for the DA-induced SAR, which is further enhanced by azelaic acid, a defense priming molecule. In response to the biological induction of SAR, DA in vascular sap is redistributed into a SAR-inducing 'signaling DA' pool that is associated with a trypsin-sensitive high molecular weight fraction, a finding that suggests that DA-orchestrated SAR involves a vascular sap protein(s).

Screening and characterization of a chemical regulator for plant disease resistance

Plants activate systemic acquired resistance (SAR), a form of long-lasting induced defense, to confer protection against a broad spectrum of pathogens. SAR induction is associated with the salicylic acid (SA)-mediated defense signaling networks. For detailed understandings of the SA-mediated signaling of SAR induction, we screened chemical inhibitors that block SA-mediated signaling from a 9600-compound chemical library. As a result, we identified one candidate chemical, 4-phenyl-2-{[3-(tri-fluoromethyl)anilino]methylidene}cyclohexane-1,3-dione (PAMD), that suppresses the expression of pathogenesis-related (PR) gene. PAMD also down-regulates SA-induced gene expression and enhances susceptibility to pathogen.

Glycerol-3-phosphate and systemic immunity

Glycerol-3-phosphate (G3P), a conserved three-carbon sugar, is an obligatory component of energy-producing reactions including glycolysis and glycerolipid biosynthesis. G3P can be derived via the glycerol kinase-mediated phosphorylation of glycerol or G3P dehydrogenase (G3Pdh)-mediated reduction of dihydroxyacetone phosphate. Previously, we showed G3P levels contribute to basal resistance against the hemibiotrophic pathogen, Colletotrichum higginsianum. Inoculation of Arabidopsis with C. higginsianum correlated with an increase in G3P levels and a concomitant decrease in glycerol levels in the host. Plants impaired in GLY1 encoded G3Pdh accumulated reduced levels of G3P after pathogen inoculation and showed enhanced susceptibility to C. higginsianum. Recently, we showed that G3P is also a potent inducer of systemic acquired resistance (SAR) in plants. SAR is initiated after a localized infection and confers whole-plant immunity to secondary infections. SAR involves generation of a signal at the site of primary infection, which travels throughout the plants and alerts the un-infected distal portions of the plant against secondary infections. Plants unable to synthesize G3P are defective in SAR and exogenous G3P complements this defect. Exogenous G3P also induces SAR in the absence of a primary pathogen. Radioactive tracer experiments show that a G3P derivative is translocated to distal tissues and this requires the lipid transfer protein, DIR1. Conversely, G3P is required for the translocation of DIR1 to distal tissues. Together, these observations suggest that the cooperative interaction of DIR1 and G3P mediates the induction of SAR in plants.

Application of acibenzolar- S-methyl and standard fungicides for control of Phytophthora blight on squash

A plant systemic acquired resistance inducer, acibenzolar- S-methyl (ASM), was evaluated to determine the efficacy for suppression of Phytophthora blight of squash caused by Phytophthora capsici under field conditions. ASM was applied as foliar sprays before and after transplanting at rates of 17.5, 8.8, and 4.4 g a.i. ha −1. Application of ASM did not significantly reduce final Phytophthora blight incidences in 2 out of 3 field experiments; however, area under the disease progress curve (AUDPC) values were reduced significantly by ASM in all experiments conducted. Disease suppression by the three application rates of ASM was not significantly different. To determine the effect of application of ASM in conjunction with standard chemical fungicides, ASM was applied with mefenoxam (Ridomil Gold), copper hydroxide, and mandipropamid (Revus). AUDPC values and final disease incidences were consistently lower in field plots treated by the combination of ASM and standard fungicides than applications of these chemicals alone. Application of ASM resulted in significantly higher squash yield than the non-treated control in 2 of 3 experiments and plots treated with the combined use of ASM and standard fungicides produced the highest yields. These results suggest that ASM may induce plant resistance under field conditions, providing suppression of Phytophthora blight of squash, and that there may be some benefit to the integration of ASM and standard chemical fungicides.

Soil Application of SAR Inducers Imidacloprid, Thiamethoxam, and Acibenzolar-S-Methyl for Citrus Canker Control in Young Grapefruit Trees.

Soil applications of inducers of systemic acquired resistance (SAR) imidacloprid, thiamethoxam, or acibenzolar-S-methyl, at various rates and application frequencies, were evaluated for control of citrus canker caused by Xanthomonas citri subsp. citri in a field trial of 3- and 4-year-old 'Ray Ruby' grapefruit trees in southeastern Florida. Reduction of foliar incidence of canker produced by one, two, or four soil applications of imidacloprid, thiamethoxam, and acibenzolar-S-methyl was compared with 11 foliar sprays of copper hydroxide and streptomycin applied at 21-day intervals. In the 2008 and 2009 crop seasons, canker incidence on each set of vegetative flushes was assessed as the percentage of the total leaves with lesions. By the end of the 2008 season, despite above-average rainfall and a tropical storm event, all treatments significantly reduced foliar incidence of citrus canker on the combined spring-summer-fall flushes. Sprays of copper hydroxide and streptomycin were effective for reducing canker incidence on shoot flushes produced throughout the season compared with the untreated control, whereas soil-applied SAR inducers reduced foliar disease depending on rate, frequency, and timing of application. Except for the treatment of four applications of acibenzolar-S-methyl at 0.2 g a.i. per tree or two applications of imidacloprid, SAR inducers were ineffective for reducing foliar disease on the flushes that were present during the tropical storm. In 2009, all treatments significantly reduced the incidence of foliar canker on the combined spring-summer-fall flushes but not all treatments of spring-summer flushes with SAR inducers were effective compared with the untreated control. Hence, depending on rate, frequency, and timing of application, soil-applied SAR inducers reduced incidence of canker on foliar flushes of young grapefruit trees under epidemic conditions.

Glycerol-3-phosphate is a critical mobile inducer of systemic immunity in plants

Glycerol-3-phosphate (G3P) is an important metabolite that contributes to the growth and disease-related physiologies of prokaryotes, plants, animals and humans alike. Here we show that G3P serves as the inducer of an important form of broad-spectrum immunity in plants, termed systemic acquired resistance (SAR). SAR is induced upon primary infection and protects distal tissues from secondary infections. Genetic mutants defective in G3P biosynthesis cannot induce SAR but can be rescued when G3P is supplied exogenously. Radioactive tracer experiments show that a G3P derivative is translocated to distal tissues, and this requires the lipid transfer protein, DIR1. Conversely, G3P is required for the translocation of DIR1 to distal tissues, which occurs through the symplast. These observations, along with the fact that dir1 plants accumulate reduced levels of G3P in their petiole exudates, suggest that the cooperative interaction of DIR1 and G3P orchestrates the induction of SAR in plants.

Systemic Acquired Resistance of Pepper to Microbial Pathogens

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.

Write 'systemic small RNAs': read 'systemic immunity'.

About 50 years ago, it was reported that pathogen-infected plants are less susceptible to a broad spectrum of the subsequent pathogen attacks. This form of induced resistance, which resembles the immunisation in mammalian cells, is called systemic acquired resistance (SAR). In the last 10 years, plant molecular biology has been revolutionised by the discovery of RNA silencing, which is also a systemic phenomenon and also contributes to plant immunity. Here, I review these two systemic phenomena in a comparative way to highlight the possibility that systemic silencing contributes to systemic immunity. This potential contribution could be in the process of gene expression reprogramming, which is needed for SAR induction, and/or in SAR signal complex, and/or in establishing SAR in remote tissues and forming priming status.

Cytoplasmic H2O2 prevents translocation of NPR1 to the nucleus and inhibits the induction of PR genes 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.

Suppressive effect of abscisic acid on systemic acquired resistance in tobacco plants

Recent studies have indicated that the phytohormone abscisic acid (ABA), induced in response to a variety of environmental stresses, plays an important role in modulating diverse plant–pathogen interactions. In Arabidopsis thaliana, we previously clarified that ABA suppressed the induction of systemic acquired resistance (SAR), a plant defense system induced by pathogen infection through salicylic acid (SA) accumulation. We investigated the generality of this suppressive effect by ABA on SAR using tobacco plants. For SAR induction, we used 1,2-benzisothiazole-3(2H)-one 1,1-dioxide (BIT) and benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester (BTH) that activate upstream and downstream of SA in the SAR signaling pathway, respectively. Wild-type tobacco plants treated with BIT or BTH exhibited enhanced disease resistance against Tobacco mosaic virus (TMV) and tobacco wildfire bacterium, Pseudomonas syringae pv. tabaci (Pst), however, which was suppressed by pretreatment of plants with ABA. Pretreatment with ABA also suppressed the expression of SAR-marker genes by BIT and BTH, indicating that ABA suppressed the induction of SAR. ABA suppressed BTH-induced disease resistance and pathogenesis-related (PR) gene expression in NahG-transgenic plants that are unable to accumulate SA. The accumulation of SA in wild-type plants after BIT treatment was also suppressed by pretreatment with ABA. These data suggest that ABA suppresses both upstream and downstream of SA in the SAR signaling pathway in tobacco.

Systemic acquired resistance is induced by R gene‐mediated responses independent of cell death

On infection by pathogens, plants initiate defence responses that are able to curtail infection locally. These responses are mediated either by receptor-like proteins that recognize pathogen-associated molecular patterns or by the protein products of disease resistance (R) genes. At the same time, primary defence responses often result in the generation of signals that induce what is known as systemic acquired resistance (SAR), such that defence responses are enhanced on secondary pathogen challenge in distal tissues. R protein-mediated SAR induction is normally accompanied by a type of programmed cell death known as the hypersensitive response (HR) and, in some instances, cell death alone has been implicated in the induction of SAR. This has raised the question of whether R protein-mediated signalling per se induces SAR or whether SAR is an indirect result of the induction of HR. Using the Rx gene of potato, which confers resistance to Potato Virus X in the absence of cell death, we have shown that the HR is dispensable for R protein-mediated induction of SAR and that Rx-induced SAR is mediated by the same salicylate-dependent pathway induced by other R proteins.

Changes of defense proteins in the extracellular proteome of grapevine (Vitis vinifera cv. Gamay) cell cultures in response to elicitors

In plant cells, elicitors induce defense responses that resemble those triggered by pathogen attack, such as the synthesis of phytoalexins and pathogen-related proteins which accumulate in the extracellular space. In the search for the particular proteins involved in defense responses, we investigated the changes in the extracellular proteome of a grapevine (Vitis vinifera cv. Gamay) cell suspension in response to elicitation with methylated cyclodextrins (MBCD) and methyl jasmonate (MeJA). Twenty-five of the 39 spots differentially expressed in 2-D gels were identified and found to be encoded by 10 different genes: three secretory peroxidases, chitinase-III, beta-1,3-glucanase, thaumatin-like, SGNH plant lipase-like, NtPR27-like, xyloglucan endotransglycosylase and subtilisin-like protease. Most of them belong to the pathogenesis-related type proteins. A new class III secretory basic peroxidase and chitinase III were strongly induced in cultures treated with MBCD alone or combined with MeJA, while cultures treated with MeJA alone displayed a general repression of most of the extracellular proteins. Some of the proteins induced in grapevine cell cultures by MBCD are induced in other species by activators of systemic acquired resistance (SAR), a form of plant immunity. Collectively, the results suggest that treatment with MBCD resembles the effect of SAR induction agents in cell cultures.

Effect of benzothiadiazole, an inducer of systemic acquired resistance, on the pathogenesis of wheat brown rust

We studied the effects of systemic acquired resistance inducer, benzothiadiazole (BT, benzo-(1,2,3-thiadiazole-7-carbothionic acid S-methyl ester, commercial name BION), on the development of brown rust caused by the fungus Puccinia triticina Erikss. in nearly isogenic lines of common wheat (Triticum aestivum L, cv. Thatcher) carrying the resistance genes Lr19 and Lr24. A dependence of BT efficiency on the time between treatment with the inducer and inoculation with urediniospores was observed. A difference in BT action on pathogenesis during wheat line infection with virulent and avirulent P. triticina clones was detected. In compatible combinations, the morphogenesis of virulent clone mycelium was suppressed without the hypersensitive response. The inhibition of the development of avirulent clone colonies was accompanied by the intense hypersensitive response. Treatment with cycloheximide enhanced avirulent clone development during 3 days after inoculation; however, later colony growth ceased.