Showing papers on "Systemic acquired resistance published in 1997"

Systemic acquired resistance

Abstract: This paper examines induced resistance (SAR) in plants against various insect and pathogenic invaders. SAR confers quantitative protection against a broad spectrum of microorganisms in a manner comparable to immunization in mammals, although the underlying mechanisms differ. Discussed here are the molecular events underlying SAR: the mechanisms involved in SAR, including lignification and other structural barriers, pathogenesis-related proteins and their expression, and the signals for SAR including salicylic acid. Recent findings on the biological role of systemin, ethylene, jasmonates, and electrical signals are reviewed. Chemical activators of SAR comprise inorganic compounds, natural compounds, and synthetic compounds. Plants known to exhibit SAR and induced systemic resistance are listed.

Induced resistance in plants and the role of pathogenesis-related proteins

Abstract: The nature of induced resistance Resistance, according to Agrios (1988) is the ability of an organism to exclude or overcome, completely or in some degree, the effect of a pathogen or other damaging factor Disease resistance in plants is manifested by limited symptoms, reflecting the inability of the pathogen to grow or multiply and spread, and often takes the form of a hypersensitive reaction (HR), in which the pathogen remains confined to necrotic lesions near the site of infection Induced resistance is the phenomenonthat a plant, once appropriately stimulated, exhibits an enhanced resistance upon 'challenge' inoculation with a pathogen Although induced resistance has been attracting attention recently (Ryals et al, 1994; Hammerschmidt and Kuc, 1995), the first systematic enquiry into induced resistance was made by Ross (1961a,b) He observed that the inducible resistance response to tobacco mosaic virus (TMV) in N gene-containing, hypersensitively reacting tobacco was not confined to the immediate vicinity of the resulting local necrotic lesions, but extended to other plant parts A ring of tissue around the developing lesions became fully refractory to subsequent infection (localized acquired resistance; Ross, 1961a), whereas challenge inoculation of distant tissues resulted in much smaller, and occasionally fewer, lesions (systemic acquired resistance (SAR); Ross, 1961b) than in non-induced plants Even leaves thatweremere initials at the time of the primary inoculation became induced, suggesting that as a result of the initial infection, a signal was generated, transported and propagated, that primed the plant to respond more effectively to subsequent infection (Bozarth and Ross, 1964) Treatments that influenced lesion size after primary infection had similar effects on lesions developing upon challenge inoculation (Ross, 1966), leading to the conclusion that the mechanisms responsible for resistance expression were the same under both conditions Only upon challenge inoculation, defense mechanisms appeared to be expressed earlier and to a greater extent (De Laat and Van Loon, 1983; Dean and Kuc, 1987)

The cpr5 mutant of Arabidopsis expresses both NPR1-dependent and NPR1-independent resistance.

Abstract: The cpr5 mutant was identified from a screen for constitutive expression of systemic acquired resistance (SAR). This single recessive mutation also leads to spontaneous expression of chlorotic lesions and reduced trichome development. The cpr5 plants were found to be constitutively resistant to two virulent pathogens, Pseudomonas syringae pv maculicola ES4326 and Peronospora parasitica Noco2; to have endogenous expression of the pathogenesis-related gene 1 (PR-1); and to have an elevated level of salicylic acid (SA). Lines homozygous for cpr5 and either the SA-degrading bacterial gene nahG or the SA-insensitive mutation npr1 do not express PR-1 or exhibit resistance to P. s. maculicola ES4326. Therefore, we conclude that cpr5 acts upstream of SA in inducing SAR. However, the cpr5 npr1 plants retained heightened resistance to P. parasitica Noco2 and elevated expression of the defensin gene PDF1.2, implying that NPR1-independent resistance signaling also occurs. We conclude that the cpr5 mutation leads to constitutive expression of both an NPR1-dependent and an NPR1-independent SAR pathway. Identification of this mutation indicates that these pathways are connected in early signal transduction steps and that they have overlapping functions in providing resistance.

The Arabidopsis NIM1 protein shows homology to the mammalian transcription factor inhibitor I kappa B.

Abstract: The NIM1 (for noninducible immunity) gene product is involved in the signal transduction cascade leading to both systemic acquired resistance (SAR) and gene-for-gene disease resistance in Arabidopsis. We have isolated and characterized five new alleles of nim1 that show a range of phenotypes from weakly impaired in chemically induced pathogenesis-related protein-1 gene expression and fungal resistance to very strongly blocked. We have isolated the NIM1 gene by using a map-based cloning procedure. Interestingly, the NIM1 protein shows sequence homology to the mammalian signal transduction factor I kappa B subclass alpha. NF-kappa B/I kappa B signaling pathways are implicated in disease resistance responses in a range of organisms from Drosophila to mammals, suggesting that the SAR signaling pathway in plants is representative of an ancient and ubiquitous defense mechanism in higher organisms.

Differential induction of systemic resistance in Arabidopsis by biocontrol bacteria

Abstract: Selected nonpathogenic, root-colonizing bacteria are able to elicit induced systemic resistance (ISR) in plants. To elucidate the molecular mechanisms underlying this type of systemic resistance, an Arabidopsis-based model system was developed in which Pseudomonas syringae pv. tomato and Fusarium oxysporum f. sp. raphani were used as challenging pathogens. In Arabidopsis thaliana ecotypes Columbia and Landsberg erecta, colonization of the rhizosphere by P. fluorescens strain WCS417r induced systemic resistance against both pathogens. In contrast, ecotype RLD did not respond to WCS417r treatment, whereas all three ecotypes expressed systemic acquired resistance upon treatment with salicylic acid (SA). P. fluorescens strain WCS374r, previously shown to induce ISR in radish, did not elicit ISR in Arabidopsis. The opposite was found for P. putida strain WCS358r, which induced ISR in Arabidopsis but not in radish. These results demonstrate that rhizosphere pseudomonads are differentially active in eliciting ISR in related plant species. The outer membrane lipopolysaccharide (LPS) of WCS417r is the main ISR-inducing determinant in radish and carnation, and LPS-containing cell walls also elicit ISR in Arabidopsis. However, mutant WCS417rOA-, lacking the O-antigenic side chain of the LPS, induced levels of protection similar to those induced by wild-type WCS417r. This indicates that ISR-inducing bacteria produce more than a single factor that trigger ISR in Arabidopsis. Furthermore, WCS417r and WCS358r induced protection in both wild-type Arabidopsis and SA-nonaccumulating NahG plants without activating pathogenesis-related gene expression. This suggests that elicitation of an SA-independent signaling pathway is a characteristic feature of ISR-inducing biocontrol bacteria.

Arabidopsis enhanced disease susceptibility mutants exhibit enhanced susceptibility to several bacterial pathogens and alterations in PR-1 gene expression.

Abstract: To identify plant defense responses that limit pathogen attack, Arabidopsis eds mutants that exhibit enhanced disease susceptibility to the virulent bacterial pathogen Pseudomonas syringae pv maculicola ES4326 were previously identified. In this study, we show that each of four eds mutants (eds5-1, eds6-1, eds7-1, and eds9-1) has a distinguishable phenotype with respect to the degree of susceptibility to a panel of bacterial phytopathogens and the ability to activate pathogenesis-related PR-1 gene expression after pathogen attack. None of the four eds mutants exhibited observable defects in mounting a hypersensitive response. Although all four eds mutants were also capable of mounting a systemic acquired resistance response, enhanced growth of P. s. maculicola ES4326 was still apparent in the secondarily infected leaves of three of the eds mutants. These data indicate that eds genes define a diverse set of previously unknown defense responses that affect resistance to virulent pathogens.

Use of arabidopsis for genetic dissection of plant defense responses

Abstract: Arabidopsis thaliana (Arabidopsis) is proving to be an ideal model system for studies of host defense responses to pathogen attack. The Arabidopsis genetic system is significantly more tractable than those of other plant species, and Arabidopsis exhibits all of the major kinds of defense responses described in other plants. A large number of virulent and avirulent bacterial, fungal, and viral pathogens of Arabidopsis have been collected. In the last few years, a large number of mutations have been identified in Arabidopsis that cause a wide variety of specific defense-related phenotypes. Analysis of these mutant phenotypes is beginning to give glimpses into the complex signal transduction pathways leading to the induction of the defense responses involved in protecting plants from pathogen infection.

Differential Expression of Chitinases in Vitis vinifera L. Responding to Systemic Acquired Resistance Activators or Fungal Challenge

Abstract: The concept of systemic acquired resistance (SAR) enables a novel approach to crop protection, and particular pathogenesis-related proteins, i.e. an acidic chitinase, have been classified as markers of the SAR response. Basic class I (VCHIT1b) and a class III (VCH3) chitinase cDNAs were cloned from cultured Vitis vinifera L. cv Pinot Noir cells and used to probe the induction response of grapevine cells to salicylic acid or yeast elicitor. Furthermore, the cells were treated with the commercial SAR activators 2,6-dichloroiso-nicotinic acid or benzo(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester. Elicitor or salicylic acid induced both VCHIT1b and VCH3 transcript abundances, whereas 2,6-dichloroiso-nicotinic acid or benzo(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester enhanced exclusively the expression of VCH3. To assess the systemic sensation of chitinase expression, single leaves of Vitis vinifera L. cv Pinot Noir or Vitis rupestris plants were inoculated with Plasmopara viticola spore suspensions, and the VCH3 and VCHIT1b mRNA amounts in the infected versus the adjacent, healthy leaf were monitored. Two VCH3 mRNA maxima were observed 2 and 6 d postinoculation in the infected, susceptible V. vinifera tissue, whereas in the healthy leaf the transcript increased from low levels d 2 postinoculation to prominent levels d 6 to 8 postinoculation. The level of VCH3 mRNA increased also over 4 d in the inoculated, resistant V. rupestris tissue. However, necrotic spots rapidly limited the infection, and the VCH3 transcript was undetectable in the upper-stage, healthy leaf. The expression of VCHIT1b remained negligible under either experimental condition. Overall, the results suggest that the selective expression of VCH3 might be a reliable indicator of the SAR response in V. vinifera L.

Fungal pathogenesis in plants and crops: molecular biology and host defense mechanisms.

Abstract: PERCEPTION AND TRANSDUCTION OF PLANT SIGNALS IN PATHOGENS Introduction Signaling and Transduction Systems in "First Touch" and Adhesion of Fungal Spores Signaling in Fungal Spore Germination Signaling in Differentiation of Germ Tubes into Infection Structures Signal Transduction in Fungal Pathogenesis Genes Involved in Formation of Infection Structures Signals in Fungal Infection Process Conclusion References PERCEPTION AND TRANSDUCTION OF PATHOGEN SIGNALS IN PLANTS Introduction What Are Elicitors? Oligosaccharide Elicitors Protein Peptide Elicitors Glycoprotein Elicitors Lipid Elicitors Toxins as Elicitor Molecules Plant Cell Wall-Degrading Enzymes as Elicitors Race-Specific and Cultivar-Specific Elicitors Specificity of General Elicitors Endogenous Oligogalacturonide Elicitors Multiple Elicitors May Be Needed to Activate Defense Responses Availability of Fungal Elicitors at the Site of Fungal Invasion in Plants Receptors for Elicitor Signals in Plant Cell Membrane Calcium Ion May Act as Second Messenger Phosphorylation of Proteins as a Component in Signal Transduction System Mitogen-Activated Protein Kinase Cascades in Signal Transduction Phospholipid-Signaling System Anion Channels in Signal Transduction Extracellular Alkalinization and Cytoplasmic Acidification in Signaling System Reactive Oxygen Species in Signal Transduction Nitric Oxide in Signal Transduction Salicylic Acid-Signaling System Jasmonate-Signaling Pathway Role of Systemin in Signal Transduction System Ethylene-Dependent Signaling Pathway Abscisic Acid Signaling Fatty Acids as Systemic Signal Molecules Other Signaling Systems Network and Interplay of Signaling Pathways Induction of Defense Genes May Require Different Signal Transduction Systems Perception and Transduction of Pathogen Signals in Plants Leading to Susceptibility Signaling Systems in Susceptible Interactions Conclusion References DISEASE RESISTANCE AND SUSCEPTIBILITY GENES IN SIGNAL PERCEPTION AND EMISSION Introduction Molecular Structure of Resistance Genes Classification of Resistance Genes based on Molecular Structure of R Gene-Encoded Proteins Molecular Structure of Recessive Genes Perception of Pathogen Signals by Resistance Genes Activation of R Protein and Emission of Signals to Other Components in the Cell Downstream Components of R Gene Signaling Systems Downstream Signaling Events in R Gene-Mediated Resistance Susceptibility Genes in Signal Transduction Conclusion References CELL DEATH PROGRAMS DURING FUNGAL PATHOGENESIS Introduction Cell Death in Resistant Interactions Molecular Mechanism of Induction of Hypersensitive Cell Death Molecular Mechanism of Induction of Spontaneous Cell Death Molecular Mechanism of Induction of Runaway Cell Death Role of Cell Death in Induction of Systemic Acquired Resistance Susceptibility-Related Cell Death Molecular Mechanisms in Induction of Cell Death in Susceptible Interactions What Is the Function of Cell Death in Fungal Pathogenesis? Conclusion References CELL WALL DEGRADATION AND FORTIFICATION Introduction Structure of Cuticle Penetration of Epicuticular Waxy Layer by Pathogens Production of Cutinases to Breach Cuticle Barrier Genes Encoding Cutinases Plant Signals Triggering Fungal Cutinases Importance of Cutinases in Penetration of Cuticle Cutinases as Virulence Pathogenicity Factors Melanins in Fungal Penetration of Cuticle Barrier Degradation of Pectic Polysaccharides Pathogens Produce Cellulolytic Enzymes to Breach Cell Wall Barrier Fungal Hemicellulases in Plant Cell Wall Degradation Degradation of Cell Wall Structural Proteins Requirement of Several Cell Wall-Degrading Enzymes to Degrade the Complex-Natured Cell Wall Production of Suitable Enzymes in Appropriate Sequence by Fungal Pathogens Reinforcement of Host Cell Wall during Fungal Invasion Papillae Suppress Fungal Penetration Callose Deposition in Cell Wall How Do Pathogens Overcome the Papillae and Callose Barriers? Cell Wall-Bound Phenolics and Lignins Suberization during Fungal Pathogenesis Deposition of Mineral Elements in Host Cell Wall in Response to Fungal Invasion Conclusion References INDUCTION AND EVASION OF PATHOGENESIS-RELATED PROTEINS Introduction Multiplicity of PR Proteins Classification of PR Proteins Induction of PR Proteins during Fungal Pathogenesis Genes Encoding PR Proteins Transcription of PR Genes Signals Involved in Transcriptional Induction of PR Genes PR Proteins Are Synthesized as Larger Precursors Secretion of PR Proteins PR Proteins May Be Involved in Inhibition of Pathogen Development PR Proteins May Be Involved in Triggering Disease Resistance How Do Pathogens Overcome Fungitoxic PR Proteins of the Host? Conclusion References EVASION AND DETOXIFICATION OF SECONDARY METABOLITES Introduction Chemical Structural Classes of Phytoalexins Biosynthesis of Isoflavonoid Phytoalexins Biosynthesis of Flavanone Phytoalexins Biosynthesis of Coumarin Phytoalexins Biosynthesis of Stilbene Phytoalexins Biosynthesis of Terpenoid Phytoalexins Biosynthesis of Indole-Based Sulfur-Containing Phytoalexins Biosynthesis of Alkaloid Phytoalexins Site of Synthesis of Phytoalexins Phytoalexins Are Fungitoxic How Do Pathogens Overcome the Antifungal Phytoalexins? Chemical Structural Classes of Phytoanticipins Phenolics as Phytoanticipins Toxicity of Phenolics to Pathogens How Does Pathogen Overcome the Antifungal Phenolics? Saponins as Phytoanticipins Glucosinolates as Phytoanticipins Cyanogenic Glucosides Dienes Conclusion References TOXINS IN DISEASE SYMPTOM DEVELOPMENT Introduction Importance of Toxins in Disease Development Toxins Suppress Host-Defense Mechanisms Toxins Cause Cell Membrane Dysfunction How Do Pathogens Induce Membrane Dysfunction only in Susceptible Hosts? Conclusion References Index

The Effects of Salicylic Acid and Tobacco Mosaic Virus Infection on the Alternative Oxidase of Tobacco

Abstract: Salicylic acid (SA) is a signal in systemic acquired resistance and an inducer of the alternative oxidase protein in tobacco (Nicotiana tabacum cv Xanthi nc) cell suspensions and during thermogenesis in aroid spadices. The effects of SA on the levels of alternative oxidase protein and the pathogenesis-related 1a mRNA (a marker for systemic acquired resistance), and on the partitioning of electrons between the Cyt and alternative pathways were investigated in tobacco. Leaves were treated with 1.0 mM SA and mitochondria isolated at times between 1 h and 3 d after treatment. Alternative oxidase protein increased 2.5-fold within 5 h, reached a maximum (9-fold) after 12 h, and remained at twice the level of control plants after 3 d. Measurements of isotope fractionation of 18O by intact leaf tissue gave a value of 23% at all times, identical to that of control plants, indicating a constant 27 to 30% of electron-flow partitioning to the alternative oxidase independent of treatment with SA. Transgenic NahG tobacco plants that express bacterial salicylate hydroxylase and possess very low levels of SA gave a fractionation of 23% and showed control levels of alternative oxidase protein, suggesting that steady-state alternative oxidase accumulates in an SA-independent manner. Infection of plants with tobacco mosaic virus resulted in an increase in alternative oxidase protein in both infected and systemic leaves, but no increase was observed in comparably infected NahG plants. Total respiration rate and partitioning of electrons to the alternative pathway in virus-infected plants was comparable to that in uninfected controls.

The Chemistry of Benzothiadiazole Plant Activators

Abstract: Systemic Acquired Resistance (SAR) is an inducible resistance mechanism in plants that, together with other defence mechanisms, provides broad-spectrum and long-lasting disease control. With novel screening techniques the benzo[1,2,3]thiadiazole-7-carboxylic acid derivatives have been identified as a new class of chemicals which stimulate the plant's own defence mechanisms. The synthesis and biological activities of various benzo[1,2,3]thiadiazoles and related structures are described. S-Methyl benzo[1,2,3]thiadiazole-7-carbothioate is the first synthetic chemical 'plant activator' that has been developed for this novel disease control concept.

Two PR-1 Genes from Tomato Are Differentially Regulated and Reveal a Novel Mode of Expression for a Pathogenesis-Related Gene During the Hypersensitive Response and Development

Abstract: Pathogenesis-related (PR) proteins form a heterogeneous family of plant proteins that are likely to be involved in defense and are inducible by pathogen attacks. One group of PRs, represented by the subfamily PR-1, are low-molecular-weight proteins of unknown biochemical function. Here we describe the cloning and characterization of two closely related genes encoding a basic and an acidic PR-1 protein (PR1b1 and PR1a2) from tomato (Lycopersicon esculentum). We present a comparative study of the mode of transcriptional regulation of these two genes in transgenic tobacco plants using a series of promoter-GUS fusions. Unexpectedly, the chimeric PR1a2/GUS gene is not induced by pathogenic signals but instead shows constitutive expression with a reproducible developmental expression pattern. It is expressed in shoot meristems, trichomes, and cortical cells as well as in vascular and nearby tissues of the mature stem. This constitutive expression pattern may represent preemption of plant defenses against potent...

RNase Activity Prevents the Growth of a Fungal Pathogen in Tobacco Leaves and Increases upon Induction of Systemic Acquired Resistance with Elicitin

Abstract: The hypersensitive response and systemic acquired resistance (SAR) can be induced in tobacco (Nicotiana tabacum L.) plants by cryptogein, an elicitin secreted by Phytophthora cryptogea. Stem application of cryptogein leads to the establishment of acquired resistance to subsequent leaf infection with Phytophthora parasitica var nicotianae, the agent of the tobacco black shank disease. We have studied early events that occur after the infection and show here that a tobacco gene encoding the extracellular S-like RNase NE is expressed in response to inoculation with the pathogenic fungus. Upon induction of SAR with cryptogein, the accumulation of NE transcripts coincided with a rapid induction of RNase activity and with the increase in the activity of at least two different extracellular RNases. Moreover, exogenous application of RNase activity in the extracellular space of leaves led to a reduction of the fungus development by up to 90%, independently of any cryptogein treatment and in the absence of apparent necrosis. These results indicate that the up-regulation of apoplastic RNase activity after inoculation could contribute to the control of fungal invasion in plants induced to SAR with cryptogein.

Characterization and Expression of Caffeoyl-Coenzyme A 3-O-Methyltransferase Proposed for the Induced Resistance Response of Vitis vinifera L

Abstract: Cell-suspension cultures of Vitis vinifera L cv Pinot Noir accumulated resveratrol upon fungal elicitation, and the activity of S-adenosyI-L-methionine:trans-caffeoyl-coenzyme A 3-O-methyl-transferase (CCoAOMT), yielding feruloyl-CoA, increased to a transient maximum at 12 to 15 h CCoAOMT cDNA was cloned from the elicited cells and was shown to encode a polypeptide highly homologous to CCoAOMTs from cells of Petroselinum species or Zinnia species The expression of the cDNA in Escherichia coli revealed that grapevine CCoAOMT methylates both caffeoyl-and 5-hydroxyferuloyl-coenzyme A and is probably involved in phenolic esterification and lignification Commercial plant activators induce the disease-resistance response of test plants and are considered to mimic the action of salicylic acid Among these chemicals, 2,6-dichloroisonicotinic acid and benzo(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester provoke systemic acquired resistance (SAR) and were also shown to induce the expression of class III chitinase in grapevine The SAR response is classified by an unchanged phenotype of tissues, but the mechanistic basis is unknown Treatment of the cultured V vinifera cells with either fungal elicitor or low concentrations of salicylic acid and 2,6-dichloroisonicotinic acid, respectively, raised the CCoAOMT or stilbene synthase transcript abundance, suggesting that grapevine is capable of the SAR response, whereas benzo(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester was ineffective The data imply for the first time (to our knowledge) that the expression of phenylpropanoid genes in grapevine is induced by SAR activators without phenotypic consequences and suggest a role for CCoAOMT and stilbene synthase in the disease-resistance response leading beyond the level of pathogenesis-related proteins as markers of the SAR

Salicylate-independent lesion formation in Arabidopsis lsd mutants.

Abstract: In many interactions of plants with pathogens, the primary host defense reaction is accompanied by plant cell death at the site of infection. The resulting lesions are correlated with the establishment of an inducible resistance in plants called systemic acquired resistance (SAR), for which salicylic acid (SA) accumulation is a critical signaling event in Arabidopsis and tobacco. In Arabidopsis, the lesions simulating disease (lsd) mutants spontaneously develop lesions in the absence of pathogen infection. Furthermore, lsd mutants express SAR marker genes when lesions are present and are resistant to the same spectrum of pathogens as plants activated for SAR by necrogenic pathogen infection. To assess the epistatic relationship between SA accumulation and cell death, transgenic Arabidopsis unable to accumulate SA due to the expression of the salicylate hydroxylase (nahG) gene were used in crosses with the dominant mutants lsd2 or lsd4. Progeny from the crosses were inhibited for SAR gene expression and disease resistance. However, these progeny retained the spontaneous cell death phenotype similar to siblings not expressing nahG. Because lesions form in the absence of SA accumulation for isd2 and lsd4, a model is suggested in which lesion formation in these two mutants is determined prior to SA accumulation in SAR signal transduction. By contrast, the loss of SAR gene expression and disease resistance in nahG-expressing lsd mutants indicates that these traits are dependent upon SA accumulation in the SAR signal transduction pathway.

Does Salicylic Acid Act as a Signal in Cotton for Induced Resistance to Helicoverpa zea

Abstract: Our previous study indicated that insect herbivory on cotton induced resistance to the cotton bollworm (Helicoverpa zea). Here we examine the role of salicylic acid as a signal in cotton for the induced resistance. Abundant evidence has accumulated showing that salicylic acid plays a key role in coordinating the expression of systemic acquired resistance against phyto-pathogens. We report that herbivory results in significant increases in foliar salicylic acid and H2O2, a response frequently observed following pathogenesis. In other well-studied systems (e.g., tobacco), salicylic acid inhibits the enzymatic decomposition of H2O2 by catalase and ascorbate peroxidase, but in cotton, salicylic acid has no effect on these enzymes in vitro. Furthermore, while herbivory enhances foliar catalase and ascorbate peroxidase activities, the application of salicylic acid or methyl salicylate to cotton plants does not affect foliar resistance to H. zea. The possible role of salicylic acid as a signal for induced resistance is discussed in light of these findings.

Characterization of acquired resistance in lesion-mimic transgenic potato expressing bacterio-opsin.

Abstract: The lesion-mimic mutants of certain plants display necrotic lesions resembling those of the hypersensitive response and activate local and systemic defense responses in the absence of pathogens. We have engineered a lesion-mimic phenotype in transgenic Russet Burbank potato plants through constitutive expression of a bacterio-opsin (bO) proton pump derived from Halobacterium halobium. Transgenic potato plants exhibiting a lesion-mimic phenotype had increased levels of salicylic acid and overexpressed several pathogenesis-related messenger RNAs, all hallmarks of systemic acquired resistance (SAR). The lesion-mimic plants also displayed enhanced resistance to the US1 isolate (A1 mating type) of a fungal pathogen, Phytophthora infestans, a causal agent of late blight disease. In contrast, little resistance was observed against the US8 isolate (A2 mating type) of this pathogen. Furthermore, a majority of the transgenic plants displaying the lesion-mimic phenotype had increased susceptibility to potato virus X...

Mechanisms of PGPR-induced resistance against pathogens

Abstract: Plant growth-promoting rhizobacteria can suppress diseases through antagonism between the bacteria and soilborne pathogens, as well as by inducing a systemic resistance in the plant against both root and foliar pathogens. Specific Pseudomonas strains induce systemic resistance in carnation, cucumber, radish, tobacco and Arabidopsis, as evidenced by an enhanced defensive capacity upon challenge inoculation. In carnation, radish and Arabidopsis, the O-antigeni c side chain of the bacterial outer membrane lipopolysaccharide acts as an inducing determinant, but other bacterial traits are also involved. Siderophores have been implicated in the induction of resistance in tobacco and Arabidopsis, and a novel type of siderophore, fluorebactin, may explain induction of resistance associated with salicylic acid (SA) in radish. Although SA induces phenotypically similar systemic acquired resistance, it is not necessary for the systemic resistance induced by most rhizobacterial strains, because this induced resistance is not associated with the accumulation of pathogenesis-related proteins and is fully expressed in Arabidopsis transformants unable to accumulate SA. Although some bacterial strains are equally effective in inducing resistance in different plant species, others show specificity, indicating specific recognition between bacteria and plants at the root surface.

Novel approaches to engineering disease resistance in crops.

Abstract: The natural defense mechanisms of plants are highly effective in preventing pathogen colonization and disease. Resistance is multi-tiered, with passive and active, constitutive and inducible elements (1, 2, 3). Physical barriers imposed by the host cell wall and cuticle act as a first line of defense (4), fortified by the constitutive expression of proteins and secondary metabolites with anti-microbial activity (5, 6). Pathogens able to breach these defenses are recognized by resistant plants, generating a rapid oxidative burst and activating host transcription of genes involved in the biosynthesis of antimicrobial phytoalexins, fungal cell wall degrading hydrolases (e.g., chitinase and glucanase), and a large number of pathogenesis-related (PR) proteins (7, 8). At the site of attack, resistant plants often exhibit a hypersensitive reaction (HR) to pathogen challenge (9, 10, 11). In these cases, host tissue undergoes a rapid, localized cell death that resembles mammalian apoptosis (12, 13). The local perception of pathogen attack is conveyed to distant tissues via a transmissible signal that involves salicylic acid (SA) (14, 15, 16, 17, 18, 19), further activating gene expression and conditioning a state known as systemic acquired resistance (SAR) (2, 3, 7, 20, 21, 22). Establishment of SAR is a powerful line of plant defense as it can provide broad-spectrum resistance against subsequent viral, bacterial and fungal challenges (3, 20, 23, 24, 25).

Multiple Disease Protection by Rhizobacteria that Induce Systemic Resistance-Reply.

Abstract: During the last few years, Kloepper and coworkers have presented impressive evidence that plant growth-promoting rhizobacteria (PGPR) can protect cucumber plants against fungal, bacterial, and viral diseases. After Wei et al. (14) described induction of systemic resistance of cucumber to Colletotrichum orbiculare by six strains of PGPR, it was repeatedly stated in abstracts of meetings and book chapters that PGPR strains with previously demonstrated induced systemic resistance (ISR) against C. orbiculare led to multiple-pathogen control. However, these strains were not specified, and the communications lacked the technical details necessary to judge whether ISR was the (sole) mechanism responsible. Only recently, two PGPR strains were described as inducing resistance against Fusarium wilt (7), angular leaf spot (8), and anthracnose (9), but the strains had different designations and were not among those used previously (14). Hence, we at first concluded that proof still needed to be provided that the same inducing bacterium could suppress diseases caused by different infectious agents through ISR. Our experiments were conducted before Liu et al. (9) provided details about the strains inducing ISR against C. orbiculare. Nevertheless, we now see that the same PGPR strains did indeed protect against a foliar fungus, a soilborne fungus, and a bacterium, and we admit that we overlooked these recent results when submitting our paper. To conclude that the mechanism responsible for suppression is ISR requires that the disease suppression is shown to be plant mediated and that it extends to plant parts that are not in contact with the inducing agent. This was neatly demonstrated for one PGPR strain in plants protected against Fusarium wilt, because a bioluminescent derivative of strain 89B-27 applied to one part of a split root system did not move to the part inoculated with Fusarium oxysporum f. sp. cucumerinum (7). The other studies did not address this question in detail, although it was mentioned that bacteria inducing systemic resistance were not translocated and did not colonize challenged leaves (6,8). We agree that this implies ISR involvement. However, application of PGPR by seed treatment or cotyledon injection does not exclude colonization of the foliar parts of plants by the bacteria, and hence, microbial antagonism also might play a role. In our studies on ISR in carnation (11), radish (3), and Arabidopsis (10), we have repeatedly shown that inducing bacteria were not recoverable from sites where plants were challenged and that the spatial separation was maintained for the duration of the experiments. Moreover, in all three plant species, ISR was induced by preparations of the bacterial lipopolysaccharide (4,12,13), ruling out any protective effects due to bacterial metabolism. Both Kloepper and coworkers and we have shown that similar strains of PGPR protect various plant species against diseases caused by different types of pathogens, and in doing so, both groups have independently validated the other’s results. PGPR-mediated ISR is an important mechanism of biological disease control, and it can be as effective as pathogen-induced systemic acquired resistance (1,2). Both Leeman et al. (5) and Wei et al. (15) have shown that PGPR are effective in reducing diseases under field conditions. This makes it even more important to further characterize the physiological, biochemical, and molecular mechanisms involved to make optimal use of ISR in plant protection.

Methods of using the nim1 gene to confer disease resistance in plants

Abstract: The invention concerns the location and characterization of a gene (designated NIM1) that is a key component of the SAR pathway and that in connection with chemical and biological inducers enables induction of SAR gene expression and broad spectrum disease resistance in plants. The NIM1 gene product is a structural homologue of the mammalian signal transduction factor IλB subclass α. The present invention exploits this discovery to provide altered forms of NIM1 that act as dominant-negative regulators of the systemic acquired resistance (SAR) signal transduction pathway. These altered forms of NIM1 confer the opposite phenotype as the nim1 mutant in plants transformed with the altered forms of NIM1, i.e. the transgenic plants exhibit constitutive SAR gene expression and a constitutive immunity (CIM) phenotype. The invention further concerns transformation vectors and processes for overexpressing the NIM1 gene in plants. The transgenic plants thus created have broad spectrum disease resistance. The present invention further concerns DNA molecules encoding altered forms of the NIM1 gene, expression vectors containing such DNA molecules, and plants and plant cells transformed therewith. The invention further concerns transformation vectors and processes for overexpressing the NIM1 gene in plants. Disclosed are vectors and processes for producing overexpression of the NIM1 gene in plants. The invention also concerns methods of activating SAR in plants and conferring to plants a CIM phenotype and broad spectrum disease resistance by transforming the plants with DNA molecules encoding altered forms of the NIM1 gene product.

Altered forms of the NIM1 gene conferring disease resistance in plants

Abstract: The NIM1 gene product is a structural homologue of the mammalian signal transduction factor IκB subclass α. The present invention exploits this discovery to provide altered forms of NIM1 that act as dominant-negative regulators of the systemic acquired resistance (SAR) signal transduction pathway. These altered forms of NIM1 confer the opposite phenotype as the nim1 mutant in plants transformed with the altered forms of NIM1; i.e., the transgenic plants exhibit constitutive SAR gene expression and a constitutive immunity (CIM) phenotype. The present invention further concerns DNA molecules encoding altered forms of the NIM1 gene, expression vectors containing such DNA molecules, and plants and plant cells transformed therewith. The invention also concerns methods of activating SAR in plants and conferring to plants a CIM phenotype and broad spectrum disease resistance by transforming the plants with DNA molecules encoding altered forms of the NIM1 gene product.

Methods and compositions for improving salicylic acid-independent systemic acquired disease resistance in plants

Abstract: The present invention provides methods and materials that enhance a plant's resistance to certain pathogens. A novel pathway is described and has been designated with the acronym, SI-SAR pathway, for salicylic acid-independent systemic acquired resistance. DNA constructs and methodologies are provided that facilitate the identification of compounds that activate this pathway. Methods are provided to enable the identification of novel genes and signaling components that are expressed when the SI-SAR pathway is activated. Transgenic plants with altered expression of these novel genes or signaling components of the pathway are expected to have enhanced resistance to plant pathogens. Also provided is a novel, pathogen-induced epoxide hydrolase that is inducible in the absence of SA.

Methods of using the nim1 gene to provide plant resistance to vegetables

Abstract: The invention concerns the location and characterization of a gene (designated NIM1) that is a key component of the SAR pathway and that in connection with chemical and biological inducers enables induction of SAR gene expression and broad spectrum disease resistance in plants. The NIM1 gene product is a structural homologue of the mammalian signal transduction factor I kappa B subclass alpha . The present invention exploits this discovery to provide altered forms of NIM1 that act as dominant-negative regulators of the systemic acquired resistance (SAR) signal transduction pathway. These altered forms of NIM1 confer the opposite phenotype as the nim1 mutant in plants transformed with the altered forms of NIM1, i.e. the transgenic plants exhibit constitutive SAR gene expression and a constitutive immunity (CIM) phenotype. The invention further concerns transformation vectors and processes for overexpressing the NIM1 gene in plants. The transgenic plants thus created have broad spectrum disease resistance. The present invention further concerns DNA molecules encoding altered forms of the NIM1 gene, expression vectors containing such DNA molecules, and plants and plant cells transformed therewith. The invention further concerns transformation vectors and processes for overexpressing the NIM1 gene in plants. Disclosed are vectors and processes for producing overexpression of the NIM1 gene in plants. The invention also concerns methods of activating SAR in plants and conferring to plants a CIM phenotype and broad spectrum disease resistance by transforming the plants with DNA molecules encoding altered forms of the NIM1 gene product.