Accumulation of H<Subscript>2</Subscript>O<Subscript>2</Subscript> in xylem fluids of cucumber stems during ASM-induced systemic acquired resistance (SAR) involves increased LOX activity and transient accumulation of shikimic acid

Systemic acquired resistance (SAR) to Colletotrichum orbiculare was induced in young cucumber (Cucumis sativus) plants within 3 h of ASM (acibenzolar-S-methyl) application onto the first leaves. A potent signal associated with significant accumulation of hydrogen peroxide in xylem fluids from severed stems appeared to be rapidly translocated from elicited lower leaves within 3 h and 6 h after treatment. Some metabolites of the shikimate, phenylpropanoid and lignin biosynthetic pathways were quantified and significant increases in the levels of shikimic acid were observed in ASM-treated plants challenge-inoculated with the anthracnose fungus. Furthermore, the expression of the 5-enolpyruvylshikimate-3-phosphate synthase gene (EPSPS) was 1.5 times higher within 12 h after ASM treatment in challenge-inoculated plants than in the untreated control. The involvement of lipoxygenase activity, shikimic acid and others such as caffeic acid in the induction of SAR is discussed.     

Mechanisms of Phosphate-induced Disease Resistance in Cucumber

Certain phosphate salts are known inducers of systemic acquired resistance (SAR). In the present study, a local spray application of dipotassium hydrogenphosphate (K₂HPO₄) was effective in inducing a high level of systemic protection in cucumber plants against anthracnose caused by Colletotrichum lagenarium. Resistance induction by K₂HPO₄ was associated with localized cell death in cucumber leaves treated with the phosphate salt. The cell death observed, subsequently resulted in the appearance of macroscopically visible, necrotic spots. Appearing lesions resembled those provoked by tobacco necrosis virus (TNV) during a hypersensitive response (HR) that leads to pathogen-induced activation of SAR. Phosphate-mediated cell death was preceeded by a rapid generation of superoxide and hydrogen peroxide. As a further consequence of phosphate application, a local and systemic increase in free and conjugated salicylic acid (SA) levels was detected. The phosphate-induced responses were also identified with a similar time range in cucumber leaves that had been pre-inoculated with TNV. In contrast, none of these responses was triggered by application of the commercial plant activator benzo[1,2,3]thiadiazole-7-carbothioic acid-S-methyl ester (BTH), which nevertheless was highly effective in inducing SAR in cucumber against anthracnose. In conclusion, the chemical SAR inducer K₂HPO₄ and the biological inducer TNV share some common early steps in signal transduction leading to SAR in cucumber, which differ from those involved in BTH-mediated SAR.     

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.     

植物对虫害的系统获得性抗性及抗虫与抗病信号途径间的相互作用

受病原体感染后,植物会获得一种持久广泛的抗性,称为系统获得性抗性,受到昆虫侵害时也会获得类似的系统获得性抗性.植物系统抗虫与抗病信号分子不同,前者是茉莉酸(JA)、甲基茉莉酸(Me-JA)或系统素,而后者是水杨酸(SA).SA介导的系统抗病信号途径与JA等介导的系统抗虫信号途径并非完全独立,而是存在所谓的"交叉对话",但"交叉对话"结果是相互促进还是抑制仍不清楚.植物系统抗性信号及其互作研究无疑会完善植物保护策略.     

Biological and molecular analyses of the acibenzolar-S-methyl-induced systemic acquired resistance in flue-cured tobacco against Tomato spotted wilt virus

Tomato spotted wilt virus (TSWV) is an economically important virus of flue-cured tobacco. Activation of systemic acquired resistance (SAR) by acibenzolar-S-methyl (ASM) in flue-cured tobacco was studied under greenhouse conditions by challenge inoculation with a severe isolate of TSWV. ASM restricted virus replication and movement, and as a result reduced systemic infection. Activation of resistance was observed within 2 days after treatment with ASM and a high level of resistance was observed at 5 days onward. Expression of the pathogenesis-related (PR) protein gene, PR-3, and different classes of PR proteins such as PR-1, PR-3, and PR-5 were detected at 2 days post-ASM treatment which inversely correlated with the reduction in the number of local lesions caused by TSWV. Tobacco plants treated with increased quantities of ASM (0.25, 0.5, 1.0, 2.0, and 4.0 g a.i./7,000 plants) showed increased levels of SAR as indicated by the reduction of both local and systemic infections by TSWV. The highest level of resistance was at 4 g a.i., but this rate of ASM also caused phytotoxicity resulting in temporary foliar spotting and stunting of plants. An inverse correlation between the TSWV reduction and phytotoxicity was observed with the increase of ASM concentration. ASM at the rate of 1 to 2 g a.i./7,000 plants activated a high level of resistance and minimized the phytotoxicity. Use of gibberellic acid in combination with ASM reduced the stunting caused by ASM. Present findings together with previous field experiments demonstrate that ASM is a potential option for management of TSWV in flue-cured tobacco.     

Systemic Accumulation of 12-oxo-phytodienoic Acid in SAR-induced Potato Plants

In potato plants induced for systemic resistance by infiltration with Pseudomonas syringae pv. maculicola, 12-oxo-phytodienoic acid (OPDA) accumulated in infiltrated leaves as well as in non-treated leaves of infected plants. In contrast, jasmonic acid (JA) levels increased only in infiltrated leaves, suggesting that the biosynthetic precursor of JA, OPDA, might play a role in systemic acquired resistance.     

Application of energy-filtering electron microscopy (EFEM) for analysis of hydrogen peroxide and lignin in epidermal walls of cucumber leaves triggered by acibenzolar-S-methyl treatment prior to inoculation with Colletotrichum orbiculare

Hydrogen peroxide (H₂O₂) and lignin induced by acibenzolar-S-methyl (ASM) during the expression of systemic acquired resistance (SAR) of cucumber plants against the fungus Colletotrichum orbiculare was analysed with electron microscopy and energy-filtering electron microscopy (EFEM). ASM pretreatment consistently led to the blockage of appressorial penetration pegs into leaves at early stages after inoculation, whereas the fungus was able to grow into the vascular tissue after distilled water pretreatment. The blocked pegs, seen frequently at epidermal pectin layers in leaves of ASM-treated plants, were surrounded by abundant electron-dense amorphous material and dots. These were identified as lignin, based on their appearance and high reactivity with KMnO₄. Lignin first appeared as an amorphous material at pectin layers, and then as dots in some areas of the material. The results showed that ASM caused SAR in leaves via faster formation of lignin within 1 day after inoculation. After CeCl₃ treatment to detect H₂O₂, H₂O₂-reactive products (cerium perhydroxides) were seen near ASM-induced lignin formation sites in pectin layers. EFEM analysis showed that Ce and O were located at the same sites as the lignin dots, suggesting that lignin was associated with sources of H₂O₂ generation. The results indicate that the faster H₂O₂ generation and lignification induced by ASM were the potential causes of SAR.     

Non-host resistance toColletotrichum lagenariumin pumpkin and squash is not primarily associated with β-1,3-glucanase and chitinase activities

Disease symptoms typical of anthracnose were observed in cucumber, pumpkin and squash after infiltrating leaves with a conidial suspension ofColletotrichum lagenarium, but symptoms developed only in cucumber when droplets of the conidial suspension were applied to the leaf surface. There was no difference in the germination of conidia or in appressorium formation on leaf surfaces of cucumber, pumpkin or squash plants; however, penetration was markedly reduced into pumpkin and squash with or without systemic acquired resistance (SAR) and into cucumber with SAR. Little β-1,3-glucanase and chitinase activities were detected in challenged pumpkin and squash leaves without symptoms even 5 days after inoculation in leaf surfaces. However, the enzymes were detected in pumpkin and squash leaves with symptoms, and activities of the enzymes were greater than those in cucumber. These results suggest that β-1,3-glucanase and chitinase activities are not primary initial defence compounds associated with non-host resistance of pumpkin and squash toC. lagenarium.     

Induced resistance to foliar diseases by soil solarization and Trichoderma harzianum

The effect of soil solarization and Trichoderma harzianum on induced resistance to grey mould (Botrytis cinerea) and powdery mildew (Podosphaera xanthii) was studied. Plants were grown in soils pretreated by solarization, T. harzianum T39 amendment or both, and then their leaves were inoculated with the pathogens. There was a significant reduction in grey mould in cucumber, strawberry, bean and tomato, and of powdery mildew in cucumber, with a stronger reduction when treatments were combined. Bacillus, pseudomonad and actinobacterial communities in the strawberry rhizosphere were affected by the treatments, as revealed by denaturing gradient gel electrophoresis fingerprinting. In tomato, treatments affected the expression of salicylic acid (SA)‐, ethylene (ET)‐ and jasmonic acid (JA)‐responsive genes. With both soil treatments, genes related to SA and ET – PR1a, GluB, CHI9 and Erf1 – were downregulated whereas the JA marker PI2 was upregulated. Following soil treatments and B. cinerea infection, SA‐, ET‐, and JA‐related genes were globally upregulated, except for the LOX genes which were downregulated. Upregulation of the PR genes PR1a, GluB and CHI9 in plants grown in solarized soil revealed a priming effect of this treatment on these genes' expression. The present study demonstrates the capacity of solarization and T. harzianum to systemically induce resistance to foliar diseases in various plants. This may be due to either a direct effect on the plant or an indirect one, via stimulation of beneficial microorganisms in the rhizosphere.     

Rhizobacteria-mediated Induced Systemic Resistance: Triggering, Signalling and Expression

Selected strains of rhizosphere bacteria reduce disease by activating a resistance mechanism in the plant named rhizobacteria-mediated induced systemic resistance (ISR). Rhizobacteria-mediated ISR resembles pathogen-induced systemic acquired resistance (SAR) in that both types of induced resistance render uninfected plant parts more resistant towards a broad spectrum of plant pathogens. Some rhizobacteria trigger the salicylic acid (SA)-dependent SAR pathway by producing SA at the root surface. In other cases, rhizobacteria trigger a different signalling pathway that does not require SA. The existence of a SA-independent ISR pathway has been demonstrated in Arabidopsis thaliana. In contrast to pathogen-induced SAR, ISR induced by Pseudomonas fluorescens WCS417r is independent of SA accumulation and pathogenesis-related (PR) gene activation but, instead, requires responsiveness to the plant hormones jasmonic acid (JA) and ethylene. Mutant analyses showed that ISR follows a novel signalling pathway in which components from the JA and ethylene response are successively engaged to trigger a defensive state that, like SAR, is controlled by the regulatory factor NPR1. Interestingly, simultaneous activation of both the JA/ethylene-dependent ISR pathway and the SA-dependent SAR pathway results in an enhanced level of protection. Thus combining both types of induced resistance provides an attractive tool for the improvement of disease control. This review focuses on the current status of our research on triggering, signalling, and expression of rhizobacteria-mediated ISR in Arabidopsis.     

Plant responses to plant growth-promoting rhizobacteria

Non-pathogenic soilborne microorganisms can promote plant growth, as well as suppress diseases. Plant growth promotion is taken to result from improved nutrient acquisition or hormonal stimulation. Disease suppression can occur through microbial antagonism or induction of resistance in the plant. Several rhizobacterial strains have been shown to act as plant growth-promoting bacteria through both stimulation of growth and induced systemic resistance (ISR), but it is not clear in how far both mechanisms are connected. Induced resistance is manifested as a reduction of the number of diseased plants or in disease severity upon subsequent infection by a pathogen. Such reduced disease susceptibility can be local or systemic, result from developmental or environmental factors and depend on multiple mechanisms. The spectrum of diseases to which PGPR-elicited ISR confers enhanced resistance overlaps partly with that of pathogen-induced systemic acquired resistance (SAR). Both ISR and SAR represent a state of enhanced basal resistance of the plant that depends on the signalling compounds jasmonic acid and salicylic acid, respectively, and pathogens are differentially sensitive to the resistances activated by each of these signalling pathways. Root-colonizing Pseudomonas bacteria have been shown to alter plant gene expression in roots and leaves to different extents, indicative of recognition of one or more bacterial determinants by specific plant receptors. Conversely, plants can alter root exudation and secrete compounds that interfere with quorum sensing (QS) regulation in the bacteria. Such two-way signalling resembles the interaction of root-nodulating Rhizobia with legumes and between mycorrhizal fungi and roots of the majority of plant species. Although ISR-eliciting rhizobacteria can induce typical early defence-related responses in cell suspensions, in plants they do not necessarily activate defence-related gene expression. Instead, they appear to act through priming of effective resistance mechanisms, as reflected by earlier and stronger defence reactions once infection occurs.     

Transgenic cucumber expressing an endogenous class III chitinase gene has reduced symptoms from Botrytis cinerea

A class III chitinase gene (CHI2) is induced in cucumber plants (Cucumis sativa L.) in response to infection by pathogenic microorganisms. Infection of Botrytis cinerea, causal agent of gray mold disease on cucumber, also induces CHI2 expression. To investigate whether CHI2 is involved in resistance to gray mold disease, transgenic cucumber plants were produced to overexpress the CHI2 gene. One line was analyzed in detail in terms of disease resistance. The transgenic cucumber plant (CC2) constitutively expressed CHI2 and reduced the symptoms of B. cinerea for 4 days after inoculation compared with nontransgenic plants. However, this inhibitory effect was not absolute, and CC2 eventually developed serious disease symptoms. Chitinase activity of the crude extract from CC2 leaves was higher than that from nontransgenic plants. A high-molecular-weight fraction containing CHI2 from CC2 leaves had fungistatic activity against B. cinerea. Interestingly, the low-molecular-weight fraction from CC2 leaves with CHI2 removed also had fungistatic activity against B. cinerea. Not only the introduced chitinase activity but also the endogenous defense reactions activated by overexpression of CHI2 may be involved in the enhanced gray mold disease resistance in CC2.     

Inhibitors of N-linked glycosylation induce systemic acquired resistance in cucumber

Localized treatment of cucumber (Cucumis sativus L. cv. Wisonsin) cotyledons with inhibitors of N-glycosylation such as tunicamycin or amphomycin resulted in systemic acquired resistance in the first leaf to the fungal pathogen Colletotrichum lagenarium. Resistance was maximal as early as 2 days after application and best results were observed when the inhibitor was used at 100 μ . The same treatment also induced salicylic acid accumulation as well as the expression of chitinase and a PR1-like protein. The systemic effect is not caused by the transport of tunicamycin, since tunicamycin was not detected in the leaves. Within 2 h after application tunicamycin inhibited N-glycosylation, but not protein synthesis as indicated by labelling experiments. The amount of large and small subunits of ribulose-1,5-bisphosphate carboxylase/oxygenase decreased after tunicamycin treatment and after pathogen inoculation and the expression of BiP, a protein localized in the endoplasmic reticulum was enhanced. The activation of defense reactions seems to be dependent and sensitive to N-linked glycosylation.     

Compost and compost water extract-induced systemic acquired resistance in cucumber and Arabidopsis

ABSTRACT A biocontrol agent-fortified compost mix, suppressive to several diseases caused by soilborne plant pathogens, induced systemic acquired resistance (SAR) in cucumber against anthracnose caused by Colletotrichum orbiculare and in Arabidopsis against bacterial speck caused by Pseudomonas syringae pv. maculicola KD4326. A peat mix conducive to soilborne diseases did not induce SAR. The population size of P. syringae pv. maculicola KD4326 was significantly lower in leaves of Arabidopsis plants grown in the compost mix compared to those grown in the peat mix. Autoclaving destroyed the SAR-inducing effect of the compost mix, and inoculation of the autoclaved mix with nonautoclaved compost mix or Pantoea agglomerans 278A restored the effect, suggesting the SAR-inducing activity of the compost mix was biological in nature. Topical sprays with water extract prepared from the compost mix reduced symptoms of bacterial speck and the population size of pathogenic KD4326 in Arabidopsis grown in the peat mix but not in the compost mix. The peat mix water extract applied as a spray did not control bacterial speck on plants grown in either mix. Topical sprays with salicylic acid (SA) reduced the severity of bacterial speck on plants in the peat mix but did not further reduce the severity of symptoms on plants in the compost mix. The activity of the compost water extract was heat-stable and passed through a 0.2-mum membrane filter. beta-1,3-Glucanase activity was low in cucumber plants grown in either mix, but when infected with C. orbiculare, this activity was induced to significantly higher levels in plants grown in the compost mix than in plants grown in the peat mix. Similar results were obtained for beta-D-glucuronidase (GUS) activity driven by a PR2 (beta-1,3-glucanase) gene promoter in transgenic Arabidopsis plants grown in the compost or peat mix. GUS activity was induced with topical sprays of the compost water extract or SA in plants not inoculated with the pathogen, suggesting that compost-induced disease suppression more than likely involved the potentiation of resistance responses rather than their activation and that compost-induced SAR differed from SAR induced by pathogens, SA, or compost water extract.     

Harpin-elicited hypersensitive cell death and pathogen resistance require the NDR1 and EDS1 genes

Plants sprayed with harpin, a bacterial protein that induces hypersensitive cell death (HCD), develop systemic acquired resistance (SAR) without macroscopic necrosis. HCD sometimes accompanies the development of resistance conferred by resistance (R) genes. In Arabidopsis, some R genes require one or both of the signalling components NDR1 and EDS1 for function. This study addresses whether HCD, NDR1 and EDS1 are required for induction of SAR by harpin. When Arabidopsis and tobacco leaves were sprayed with harpin, microscopic hypersensitive response (micro-HR) lesions developed. Systemic expression of PR genes and the development of resistance were accompanied by micro-HR, except in the ndr1-1 mutant, in which harpin induced micro-HR without the development of resistance or expression of the PR-1 gene. Cell death and resistance did not occur following treatment with harpin in plants that could not accumulate salicylic acid. Harpin also failed to induce resistance in Arabidopsis eds1-1 mutants. Therefore, harpin-induced resistance seems to develop concomitantly with cell death and resistance requires NDR1 and EDS1.     

Biocontrol activity and primed systemic resistance by compost water extracts against anthracnoses of pepper and cucumber

We investigated direct and indirect effects of compost water extracts (CWEs) from Iljuk-3, Iljuk-7, Shinong-8, and Shinong-9 for the control of anthracnoses caused by Colletotrichum coccodes on pepper and C. orbiculare on cucumber. All tested CWEs significantly (P < 0.05) inhibited in vitro conidial germination and appressorium formation of the fungal pathogens; however, DL-β-amino-n-butyric acid (BABA) failed to inhibit the conidial development of the pathogens. Direct treatments of the CWEs and BABA on pepper and cucumber leaves at 1 and 3 days before or after inoculation significantly (P < 0.05) reduced anthracnose severities; Iljuk-3, Shinong-9, and BABA for pepper and Iljuk-7 for cucumber had more protective activities than curative activities. In addition, root treatment of CWEs suppressed anthracnoses on the plants by the pathogens; however, CWE treatment on lower leaves failed to reduce the diseases on the upper leaves of the plants. The CWE root treatments enhanced not only the expression of the pathogenesis-related (PR) genes CABPR1, CABGLU, CAChi2, CaPR-4, CAPO1, and CaPR-10 in pepper and PR1-1a, PR-2, PR-3, and APOX in cucumber but also the activity of β-1,3-glucanase, chitinase, and peroxidase and the generation of hydrogen peroxide in pepper and cucumber under pathogen-inoculated conditions. However, the CWE treatments failed to induce the plant responses under pathogen-free conditions. These results indicated that the CWEs had direct effects, reducing anthracnoses by C. coccodes on pepper leaves and C. orbiculare on cucumber leaves through protective and curative effects. In addition, CWE root treatments could induce systemic resistance in the primed state against pathogens on plant leaves that enhanced PR gene expression, defense-related enzyme production, and hydrogen peroxide generation rapidly and effectively immediately after pathogen infection. Thus, the CWEs might suppress anthracnoses on leaves of both pepper and cucumber through primed (priming-mediated) systemic resistance.     

Colonization of <Emphasis Type="Italic">Arabidopsis</Emphasis> roots by <Emphasis Type="Italic">Trichoderma atroviride</Emphasis> promotes growth and enhances systemic disease resistance through jasmonic acid/ethylene and salicylic acid pathways

Trichoderma spp. are common soil fungi used as biocontrol agents due to their capacity to produce antibiotics, induce systemic resistance in plants and parasitize phytopathogenic fungi of major agricultural importance. The present study investigated whether colonization of Arabidopsis thaliana seedlings by Trichoderma atroviride affected plant growth and development. Here it is shown that T. atroviride promotes growth in Arabidopsis. Moreover, T. atroviride produced indole compounds in liquid cultures. These results suggest that indoleacetic acid-related indoles (IAA-related indoles) produced by T. atroviride may have a stimulatory effect on plant growth. In addition, whether colonization of Arabidopsis roots by T. atroviride can induce systemic protection against foliar pathogens was tested. Arabidopsis roots inoculation with T. atroviride provided systemic protection to the leaves inoculated with bacterial and fungal pathogens. To investigate the possible pathway involved in the systemic resistance induced by T. atroviride, the expression profile of salicylic acid, jasmonic acid/ethylene, oxidative burst and camalexin related genes was assessed in Arabidopsis. T. atroviride induced an overlapped expression of defence-related genes of SA and JA/ET pathways, and of the gene involved in the synthesis of the antimicrobial phytoalexin, camalexin, both locally and systemically. This is the first report where colonization of Arabidopsis roots by T. atroviride induces the expression of SA and JA/ET pathways simultaneously to confer resistance against hemibiotrophic and necrotrophic phytopathogens. The beneficial effects induced by the inoculation of Arabidopsis roots with T. atroviride and the induction of the plant defence system suggest a molecular dialogue between these organisms.     

Induction of systemic resistance to<Emphasis Type="Italic">Colletotrichum lindemuthianum</Emphasis> in bean by a benzothiadiazole derivative and rhizobacteria

Plants have developed mechanisms to resist secondary infection upon inoculation with a necrotizing pathogen, chemical treatment as well as treatment with some non-pathogenic microorganisms such as rhizosphere bacteria. This phenomenon has been variously described as induced systemic resistance (ISR) or systemic acquired resistance. In the present study, the chemical benzo(1,2,3)thiadiazole-7-carbothioic acid-S-methyl ester (BTH, acibenzolar-S-methyl), and the rhizobacteriaPseudomonas aeruginosa KMPCH andP. fluorescens WCS417 were tested for their ability to induce resistance toColletotrichum lindemuthianum in susceptible and moderately resistant bean plants (Phaseolus vulgaris L.). BTH induced local and systemic resistance when bean leaves were immersed in 10⁻³ to 10⁻⁷ M BTH 3 days before the challenge inoculation. At a high concentration (10⁻³ M), BTH induced resistance of the same order as resistance induced by the pathogenC. lindemuthianum, although at this high concentration BTH appeared to be phytotoxic. Soil and seed treatment with 1 mg kg⁻¹ BTH protected beans against anthracnose. BTH-mediated induced resistance was effective in susceptible and moderately resistant plants.P. aeruginosa KMPCH induced resistance in bean againstC. lindemuthianum only in a moderately resistant interaction. KMPCH-567, a salicylic acid mutant of KMPCH, failed to induce resistance, indicating that salicylic acid is important for KMPCH to induce resistance in the bean—C. lindemuthianum system.P.fluorescens WCS417 could induce resistance toC. lindemuthianum in a susceptible and in moderately resistant interactions. http://www.phytoparasitica.org posting Jan. 16, 2002.     

Possible involvement of salicylic acid in systemic acquired resistance ofCucumis sativus againstSphaerotheca fuliginea

The possible involvement of salicylic acid in systemic acquired resistance ofCucumis sativus againstSphaerotheca fuliginea was studied. Cucumber plants were inoculated with tobacco necrosis virus on the cotyledons and the level of endogenous salicylic acid in the first true leaf was determined by gas chromatography. Salicylic acid increased continously from the second day after virus inoculation to the fifth day, when the same leaf was inoculated withSphaerotheca fuliginea. In healthy plants, the efficiency of exogenous salicylic acid in inducing resistance was assayed by applying aqueous solutions at different times beforeSphaerotheca fuliginea inoculation. To evaluate the level of induced resistance, the following parameters were examined by light microscopy: percentage of conidial germination, length of the hyphae derived from single conidia, number of haustoria, percentage of epidermal cells with lignified walls and of necrotic cells underlying fungal hyphae. In treated plants conidial germination was reduced, the total length of the hyphae was shorter, the number of haustoria was lower and the haustorium-containing epidermal cells had more frequently lignified walls. Moreover, an evident increase in callose deposition was observed leading to the formation of oversized papillae around the penetration pegs. These results indicate that the application of salicylic acid before inoculation withSphaerotheca fuliginea reduces the intensity of the infectious process and that salicylic acid is involved in the expression of systemic resistance in cucumber challenged by the biotrophic pathogenSphaerotheca fuliginea.     

Pathogenesis-related proteins and acquired systemic resistance: Causal relationship or separate effects?

This paper questions whether pathogenesis-related proteins (PRs) have any role in acquired systemic resistance, and whether there may be alternative explanations for the reduced number and size of lesions formed when leaves containing PRs are inoculated with virus. It is concluded that PRs may not play a direct role in acquired resistance; that altered lesion number may result from altered susceptibility of the leaf to mechanical inoculation, and that reduced lesion size could reflect a non-specific modulation of the basic localization mechanism. Preliminary experiments showing changes in ultrastructure of leaves associated with the development of acquired systemic resistance are discussed. The most striking change was development of myelinic bodies, generally between the cell wall and plasmalemma in uninoculated areas of leaf opposite halves bearing lesions.