Search

Disease resistance in plants is often controlled by a gene-for-gene mechanism in which avirulence (avr) gene products encoded by pathogens are specifically recognized, either directly or indirectly, by plant disease resistance (R) gene products. Members of the NBS-LRR class of R genes encode proteins containing a putative nucleotide binding site (NBS) and carboxyl-terminal leucine-rich repeats (LRRs). Generally, NBS-LRR proteins do not contain predicted transmembrane segments or signal peptides, suggesting they are soluble cytoplasmic proteins. RPM1 is an NBSLRR protein from Arabidopsis thaliana that confers resistance to Pseudomonas syringae expressing either avrRpm1 or avrB. RPMI protein was localized by using an epitope tag. In contrast to previous suggestions, RPM1 is a peripheral membrane protein that likely resides on the cytoplasmic face of the plasma membrane. Furthermore, RPM1 is degraded coincident with the onset of the hypersensitive response, suggesting a negative feedback loop controlling the extent of cell death and overall resistance response at the site of infection.

Plant disease resistance (R) genes confer race-specific resistance to pathogens and are genetically defined on the basis of intra-specific functional polymorphism. Little is known about the evolutionary mechanisms that generate this polymorphism. Most R loci examined to date contain alternate alleles and/or linked homologs even in disease-susceptible plant genotypes. In contrast, the resistance to Pseudomonas syringae pathovar maculicola (RPM1) bacterial resistance gene is completely absent (rpm1-null) in 5/5 Arabidopsis thaliana accessions that lack RPM1 function. The rpm1-null locus contains a 98-bp segment of unknown origin in place of the RPM1 gene. We undertook comparative mapping of RPM1 and flanking genes in Brassica napus to determine the ancestral state of the RPM1 locus. We cloned two B. napus RPM1 homologs encoding hypothetical proteins with [approximately equal to]81% amino acid identity to Arabidopsis RPM1. Collinearity of genes flanking RPM1 is conserved between B. napus and Arabidopsis. Surprisingly, we found four additional B. napus loci in which the flanking marker synteny is maintained but RPM1 is absent. These B. napus rpm1-null loci have no detectable nucleotide similarity to the Arabidopsis rpm1-null allele. We conclude that RPM1 evolved before the divergence of the Brassicaceae and has been deleted independently in the Brassica and Arabidopsis lineages. These results suggest that functional polymorphism at R gene loci can arise from gene deletions.

Resistance to citrus tristeza virus (CTV) was evaluated in 554 progeny of 10 populations derived from Poncirus trifoliata. A dominant gene (Ctv) controlled CTV resistance in P. trifoliata. Twenty-one dominant PCR-based DNA markers were identified as linked to Ctv by bulked segregant analysis. Of the 11 closest markers to Ctv, only 2 segregated in all populations. Ten of these markers were cloned and sequenced, and codominant RFLP markers were developed. Seven RFLP markers were then evaluated in 10 populations. Marker orders were consistent in all linkage maps based on data of single populations or on combined data of populations with similar segregation patterns. In a consensus map, the six closest marker loci spanned 5.3 cM of the Ctv region. Z16 cosegregated with Ctv. C19 and AD08 flanked Ctv at distances of 0.5 and 0.8 cM, respectively. These 3 markers were present as single copies in the Poncirus genome, and could be used directly for bacterial artificial chromosome library screening to initiate a walk toward Ctv. BLAST searches of the GenBank database revealed high sequence similarities between 2 markers and known plant disease resistance genes, indicating that a resistance gene cluster exists in the Ctv region in P. trifoliata.

The Arabidopsis genes EDS1 and NDR1 were shown previously by mutational analysis to encode essential components of race-specific disease resistance. Here, we examined the relative requirements for EDS1 and NDR1 by a broad spectrum of Resistance (R) genes present in three Arabidopsis accessions (Columbia, Landsberg-erecta, and Wassilewskija). We show that there is a strong requirement for EDS1 by a subset of R loci (RPP2, RPP4, RPP5, RPP21, and RPS4), conferring resistance to the biotrophic oomycete Peronospora parasitica, and to Pseudomonas bacteria expressing the avirulence gene avrRps4. The requirement for NDR1 by these EDS1-dependent R loci is either weak or not measurable. Conversely, three NDR1-dependent R loci, RPS2, RPM1, and RPS5, operate independently of EDS1. Another RPP locus, RPP8, exhibits no strong exclusive requirement for EDS1 or NDR1 in isolate-specific resistance to P. parasitica, although resistance is compromised weakly by eds1. Similarly, resistance conditioned by two EDS1-dependent RPP genes, RPP4 and RPP5, is impaired partially by ndr1, implicating a degree of pathway cross-talk. Our results provide compelling evidence for the preferential utilization of either signaling component by particular R genes and thus define at least two disease resistance pathways. The data also suggest that strong dependence on EDS1 or NDR1 is governed by R protein structural type rather than pathogen class.

Cell suspension cultures of parsley (Petroselinum crispum) have previously been used as a suitable system for studies of the nonhost resistance response to Phytophthora sojae. In this study, we replaced the penetrating fungus by local mechanical stimulation by using a needle of the same diameter as a fungal hypha, by local application of a structurally defined fungus-derived elicitor, or by a combination of the two stimuli. Similar to the fungal infection hypha, the local mechanical stimulus alone induced the translocation of cytoplasm and nucleus to the site of stimulation, the generation of intracellular reactive oxygen intermediates (ROI), and the expression of some, but not all, elicitor-responsive genes. When the elicitor was applied locally to the cell surface without mechanical stimulation, intracellular ROI also accumulated rapidly, but morphological changes were not detected. A combination of the mechanical stimulus with simultaneous application of low doses of elicitor closely simulated early reactions to fungal infection, including cytoplasmic aggregation, nuclear migration, and ROI accumulation. By contrast, cytoplasmic rearrangements were impaired at high elicitor concentrations. Neither papilla formation nor hypersensitive cell death occurred under the conditions tested. These results suggest that mechanical stimulation by the invading fungus is responsible for the observed intracellular rearrangements and may trigger some of the previously demonstrated changes in the activity of elicitor-responsive genes, whereas chemical stimulation is required for additional biochemical processes. As yet unidentified signals may be involved in papilla formation and hypersensitive cell death.

Disease resistance in transgenic plants has been improved, for the first time, by the insertion of a gene from a biocontrol fungus. The gene encoding a strongly antifungal endochitinase from the mycoparasitic fungus Trichoderma harzianum was transferred to tobacco and potato. High expression levels of the fungal gene were obtained in different plant tissues, which had no visible effect on plant growth and development. Substantial differences in endochitinase activity were detected among transformants. Selected transgenic lines were highly tolerant or completely resistant to the foliar pathogens Alternaria alternata, A. solani, Botrytis cinerea, and the soilborne pathogen Rhizoctonia solani. The high level and the broad spectrum of resistance obtained with a single chitinase gene from Trichoderma overcome the limited efficacy of transgenic expression in plants of chitinase genes from plants and bacteria. These results demonstrate a rich source of genes from biocontrol fungi that can be used to control diseases in plants.

The southwestern corn borer (SWCB, Diatraea grandiosella Dyar) and sugarcane borer (SCB, Diatraea saccharalis Fabricius) are two related insect species that cause serious damage in maize production in subtropical and tropical regions of Central and Latin America. We analyzed quantitative trait loci (QTL) involved in resistance to the first generation of both borer species in two recombinant inbred line (RIL) populations from crosses CML131 (susceptible) x CML67 (resistant) and Ki3 (susceptible) x CML139 (resistant). Resistance was evaluated as leaf feeding damage (LFD) in replicated field trials across several environments under artificial infestation. Leaf protein concentration and leaf toughness were evaluated in one environment as putative components of resistance. The method of composite interval mapping was employed for QTL detection with RFLP linkage maps derived for each population of RIL. Estimates of the genotypic and genotype x environment interaction variances for SWCB LFD and SCB LFD were highly significant in both populations. Heritabilities ranged from 0.50 to 0.75. In Population CML131 x CML67, nine and eight mostly identical QTL were found for SWCB LFD and SCB LFD, respectively, explaining about 52% of the phenotypic variance (dr2) for each trait. In Population Ki3 x CML139, five QTL for SWCB LFD were detected, explaining 35.5% of ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]). Several of these QTL were found in regions containing QTL for leaf protein concentration or leaf toughness. A low number of QTL in common between the two RIL populations and between RIL and corresponding populations of [F.sub.2:3] indicated that the detection of QTL depended highly on the germplasm and population type. Consequently, chances of successful application of marker-based selection (MBS) for corn borer resistance are reduced when QTL are not identified in the germplasm in which the final selection will be carried out., The related insect species southwestern corn borer and sugarcane borer are among the most important lepidopteran pests affecting maize production in Central and South America. First generation larvae of both [...]

The Cf genes in tomatoes are responsible for resistance against Cladosporidium fulvum. There are several copies of this gene and 11 of these copies were analyzed for amino acid composition. Results revealed seven hypervariable amino acid residues in the leucine-rich domain. The predicted structure of the protein exposes these residues to the solvent. Further analysis of this domain reveals selection for sequence diversification.

Effects of the flower-infecting smut fungus Ustilago cynodontis on the growth, survival, and competitiveness of the clonal rhizomatous perennial grass Cynodon dactylon were explored through a series of glasshouse experiments. Ustilago cynodontis sterilized C. dactylon by replacing floral structures with a teliospore-producing fungal stroma. Infection caused a reduction in overall dry matter production and the growth rate of stolons, changed the allocation of resources between roots and shoots, and affected the survival of C. dactylon plants growing in pots under crowded conditions in a naturally lit glasshouse. In mixtures of healthy and infected plants, the growth of infected ones was disproportionally affected. Infection had no effect on the germination or emergence of seedlings. Transmission of the pathogen along stolons was incomplete, especially as the length of the stolon increased. The nutrient status of the soil had no significant effect on stolon growth. Results are discussed in terms of the differential effect of systemic floral smut diseases on tiller-forming and clonal rhizomatous perennial grasses. Key words: clonal plant; Cynodon; Gramineae; growth; smut; systemic disease; Ustilaginaceae; Ustilago.

Disease resistance in plants is commonly specified by genetically paired plant resistance (R) and pathogen avirulence (Avr) proteins. Recent molecular analyses of several R-Avr protein interactions provide compelling evidence for a receptor-ligand mechanism in which specific binding of the Avr elicitor by its matching R protein leads to activation of the plant defence response. Direct R-Avr protein recognition precedes the function of an expanding battery of plant resistance signalling components.

Botrytis is a widely known fungi group that causes disease in plants. Botrytis cinerea is one of the most important species of the genus and infects a diversified range of plants in many geographical areas. The pathogen invades the plant tissues either directly or via wounds. The interaction between plant hosts and Botrytis cinerea is reviewed. The possibility of reducing the plants' susceptibility to infection is discussed.

The role of methyl salicylate (MeSA) in the defense response of plants is investigated. MeSA is a major volatile compound produced by tobacco plants injected with tobacco mosaic virus. It is synthesized from salicylic acid. It may act as an airborne signal which activates disease resistance and the expression of genes related to defense in nearby plants and in the healthy tissues of the infected plant.

The resistance to the root-knot nematode, Meloidogyne javanica, is determined by a recessive gene, mj, in Cucumis sativus var. hardwickii. A cross between the resistant LJ 90430 and the susceptible Sumter produces the susceptible F(sub 1) offsprings, which give a segregation ratio of 1 resistant: 3 susceptible in the F(sub 2) generation. The resistance remains unaffected by cytoplasmic or maternal effects. Cross between LJ 90430 and five cucumber inbred lines indicates that the inheritance of resistance is unaffected by genetic background.

Future maize (Zea mays L.) productivity increases require breeding materials with high grain yield potential and multiple disease resistance. As part of an integrated program to develop breeding populations with high grain yield potential and multiple disease resistance, two maize synthetics were reciprocally recurrently selected for yield and mass selected for multiple disease resistance. The objective of this study was to determine selection response of two maize synthetics to six cycles of tandem selection for multiple leaf diseases (MLD) and multiple stalk rots (MSR). Plants were inoculated each cycle and evaluated for MLD including their causal agents; northern corn leaf blight, (NCLB) [Exserohilum turcicum (Pass.) Leonard and Suggs, Races 0 and 1], southern corn leaf blight (SCLB) [Bipolaris maydis (Nisik) Shoem.], northern corn leaf spot (NCLS) [Bipolaris zeicola (Stout) Shoem. Races 1, 2, and 31, anthracnose leaf blight [Colletrotirchum graminicola (CES) G. W. Wils.], and eyespot (Kabadella zeae Narita and Hiratsuka). Following anthesis, plants were inoculated and evaluated for resistance to MSR including their causal agents; diplodia stalk rot (DSR) [Stenocarpella maydis (BERK) Sutton = syn. Diploidia maydis (BERK)], anthracnose stalk rot (ASR) (Colletotrichum graminiscola), gibberella stalk rot (GSR) [Gibberella zeae (Shw.) Petch.], and fusarium stalk rot [Fusarium moniloforme, Shield). In 1993 and 1994, selection cycles 0, 2, 4, and 6 of synthetics RSSSC, RBS10, and their cycle crosses were evaluated. Selection response to MLD, NCLB, SCLB, NCLS, gray leaf spot (GLS; Cercospora zeae-maydis Tehon and Daniels), MSR, DSR, GSR, and ASR were measured in separate experiments. Decreases in leaf blight severity from Co to [C.sub.6] in RSSSC was 29% for MLD, 23% for NCLB, 33% for SCLB, 28% for NCLS, and 21% for GLS. Decreases for RBS10 were 34% for MLD, 33% for NCLB, 37% for SCLB, 49% for NCLS, and 16% for GLS. Cycle crosses were usually intermediate in values for leaf blight reductions. For stalk rots, the reduction in percentage internode area discolored from [C.sub.0] to [C.sub.6] for RSSSC was 44% for MSR, 42% for DSR, 39% for GSR, and 18% for ASR. Reductions for RBS10 were 63% for MSR, 67% for DSR, 64% for GSR, and 63% for ASR. Selection for multiple disease resistance along with a reciprocal recurrent program for yield resulted in significant improvement in resistance to multiple and individual diseases in RSSSC, RBS10, and their crosses., From 1950 TO 1980, genetic improvement of maize hybrids was estimated to be 92 kg [ha.sup.-1] [yr.sup.-1]. Yield gains were associated with consistent reductions in root and stalk lodging, reduction [...]

The Arabidopsis thaliana disease resistance genes RPS2 and RPM1 belong to a class of plant disease resistance genes that encode proteins that contain an N-terminal tripartite nucleotide binding site (NBS) and a C-terminal tandem array of leucine-rich repeats. RPS2 and RPM1 confer resistance to strains of the bacterial phytopathogen Pseudomonas syringae carrying the avirulence genes avrRpt2 and avrB, respectively. In these gene-for-gene relationships, it has been proposed that pathogen avirulence genes generate specific ligands that are recognized by cognate receptors encoded by the corresponding plant resistance genes. To test this hypothesis, it is crucial to know the site of the potential molecular recognition. Mutational analysis of RPS2 protein and in vitro translation/translocation studies indicated that RPS2 protein is localized in the plant cytoplasm. To determine whether avirulence gene products themselves are the ligands for resistance proteins, we expressed the avrRpt2 and avrB genes directly in plant cells using a novel quantitative transient expression assay, and found that expression of avrRpt2 and avrB elicited a resistance response in plants carrying the corresponding resistance genes. This observation indicates that no bacterial factors other than the avirulence gene products are required for the specific resistance response as long as the avirulence gene products are correctly localized. We propose that molecular recognition of P. syringae in RPS2- and RPM1-specified resistance occurs inside of plant cells.

Genetic markers linked with quantitative trait loci (QTL) may enable indirect selection of complex disease resistance. Construction of separate linkage maps to identify QTL for each complex disease resistance trait of common bean (Phaseolus vulgaris L.) is unfeasible, however. We investigated whether selective mapping could be used to hasten identification of random amplified polymorphic DNA (RAPD) associated with QTL conditioning bean golden mosaic virus (BGMV) or common bacterial blight (CBB) resistance. The mapping population ('Dorado' x XAN 176) consisted of 79 [F.sub.5:7] recombinant inbred lines. A bulked segregant analysis (BSA) of as few as three individuals and selective genotyping was used. The 101 RAPDs identified between the parents were tested across resistant vs. susceptible bulks for BGMV reaction, combined greenhonse (leaf) and field reactions to CBB, and pod (greenhouse) reaction to CBB. Fourteen of 22 RAPDs selectively mapped because they cosegregated among lines within bulks, were linked with seven of the nine QTL conditioning resistance as identified by QTL mapping using all 101 RAPDs. The two QTL not identified by this approach had minor effects. BSA and selective genotyping required only about one-third the cost and labor of completely classifying the whole population with each marker and was similarly effective for identifying RAPD markers associated with major-effect QTL that condition disease resistance in common bean. Two-locus models ([R.sup.2]), for select environments, explained 60% of the phenotypic variation in BGMV reaction, and 65, 58, and 46% of the phenotypic variation in greenhouse-leaf, -pod, and field reactions to CBB. Repulsion linkages between QTL for BGMV and CBB may complicate the combination of resistance alleles for these two traits.

The host gene Prf was found to encode a protein with leucine-zipper, nucleotide-binding and leucine-rich repeat motifs in tomato. Four prf mutant alleles were found to carry alterations within the Prf coding sequence, and a genomic fragment containing Prf was found to complement a prf mutant tomato line for sensitivity to the insecticide Fenthion and for resistance to Pst strains expressing avrPto. In addition, Prf was found to reside in the center of the Pto gene cluster, 500 bp from the Fen gene and 24 kb from the Pto gene.

Screening of cowpea [Vigna unguiculata (L.) Walp.] germplasm for additional resistance to the root-knot nematodes, Meloidogyne incognita (Kofoid and White) Chitwood and M. javanica (Treub) Chitwood, revealed an accession (IT84S-2049) from Africa with resistance to diverse populations of both root-knot species. The resistance was effective against nematode isolates that are virulent to the resistance gene Rk present in commercial cowpea cultivars, in addition to isolates of gene Rk-avirulent populations. This study was conducted to elucidate the inheritance of a newly identified, highly effective source of resistance, and to determine its relationship to gene Rk in existing cultivars. Egg mass production on root systems of plants in growth pouches was used to assess susceptibility-resistance of [F.sub.1], [F.sub.2], [F.sub.3], [BC.sub.1][F.sub.1], [BC.sub.1][F.sub.2], and [TC.sub.1] populations generated from crosses of IT84S-2049 with California Blackeye no. 3 (CB3, susceptible), CB5, or CB46 (both possessing Rk). Segregation of resistance to gene Rk-virulent M. incognita in progenies from IT84S-2049 x CB3 showed that resistance in IT84S-2049 is governed by one dominant nuclear gene. No susceptible recombinants were found among 1206 [F.sub.2] and 1144 [TC.sub.1] progeny from IT84S-2049 x CB5 or CB46 and inoculated with Rk-avirulent M. incognita (used to detect both resistance phenotypes). Resistance in IT84S-2049 is conferred by an additional dominant allele of the Rk locus, or by another gene locus very tightly linked to Rk within 0.17 map units. We propose the symbol [Rk.sup.2] to designate this new resistance factor in IT84S-2049. Thus, Rk may be a complex nematode resistance locus, analogous to those reported for other plant pathogen-host combinations.

Black root rot, caused by Chalara elegans Nag. Raj and Kendrick (syn: Thielaviopsis basicola [Berk. and Broome] Ferr.), is a common soil-borne fungal disease in cultivated tobacco (Nicotiana tabacum L., 2n = SSTT = 48). Only polygenic partial resistance to this disease is available in the original tobacco genomes; however, Nicotiana debneyi Domin, a tetraploid relative of tobacco (2n = XXYY = 48) has complete resistance to a wide spectrum of black root rot biotypes. A fertile somatic hybrid between N. tabacum 'Delgold' and N. debneyi was previously produced and was used to transfer the N. debneyi black root rot resistance into tobacco. Tobacco addition lines carrying the N. debneyi chromosomes with the gene for black root rot resistance were produced after two generations of backcrossing to the recurrent tobacco parent followed by two generations of selfing. Random amplified polymorphic DNA (RAPD) analyses of the disomic (2n = 50) addition lines and 14 monosomic (2n = 49) addition lines derived there from provided strong evidence that the two N. debneyi chromosomes in the 2n = 50 addition lines were identical. However, the tobacco genetic background apparently prevented homologous pairing of these chromosomes or caused their desynapsis. Lagging chromosomes at anaphase I and micronuclei at telophase I were observed. Transmission rates of the N. debneyi chromosomes through the egg and pollen of the addition lines were 8.1 and 10.1%, respectively. The N. debneyi chromosomes in the addition lines occasionally paired with tobacco chromosomes, and therefore, translocation lines with black root rot resistance (2n = 24 II) may be obtained in the self-pollinated progeny by crossing-over. Seventeen RAPD markers were found to be associated with the N. debneyi chromosomes in the addition lines and these should be useful in monitoring further transfer of N. debneyi chromosome fragments into the tobacco genomes.

The fungal ribosome-inactivating protein, restrictocin, hampers insect feeding on Aspergillus restrictus and may be useful as an insect control agent. An experiment shows that the addition of pure restrictocin to insect diet at 1000 ppm kills 38.5% of Carpophilus freemani (C. freemani) larvae and 62.5% of Spodoptera frugiperda larvae in 48 hrs. However, the protein has no effect on C. freemani adults. C. freemani consume very little phialides with developing spores of Aspergillus restrictus compared to those with Aspergillus nidulans.

The Corngrass1 (Cg1) mutation increases the juvenile-vegetative phase length and postpones the development of resistance to common rust and European corn borer in maize. Resistance in Cg1 mid-whorl leaves is comparable to that of Cg1 and wild-type seedling leaves. Resistance in wild-type mid-whorl leaves however is different from those in other leaf types. The resistance in Cg1 mid-whorl leaves is between that in wild-type seedling and wild-type mid-whorl leaves. The results of the study show that heterochrony is probably responsible for disease and insect resistance in normal maize populations.

Genomic mapping has been used to identify a region of the host genome that determines resistance to fusiform rust disease in loblolly pine where no discrete, simply inherited resistance factors had been previously found by conventional genetic analyses over four decades. A resistance locus, behaving as a single dominant gene, was mapped by association with genetic markers, even though the disease phenotype deviated from the expected Mendelian ratio. The complexity of forest pathosystems and the limitations of genetic analysis, based solely on phenotype, had led to an assumption that effective long-term disease resistance in trees should be polygenic. However, our data show that effective long-term resistance can be obtained from a single qualitative resistance gene, despite the presence of virulence in the pathogen population. Therefore, disease resistance in this endemic coevolved forest pathosystem is not exclusively polygenic. Genomic mapping now provides a powerful tool for characterizing the genetic basis of host pathogen interactions in forest trees and other undomesticated organisms, where conventional genetic analysis often is limited or not feasible.

Bacterial streak caused by Xanthomonas campestris pv. translucens reduces yield of wheat [Triticum aestivum (L.) em Thell] worldwide. Attempts to control the disease with bactericides have been unsuccessful. Resistant cultivars offer the best protection against yield loss, but little is known about the inheritance of resistance. The objectives of this study were to estimate the heritability of resistance to bacterial streak in soft red winter wheat and to derive an effective strategy for selecting resistant genotypes. About 60 [F.sub.2:3] and [F.sub.2:4] lines from each of three populations (Pop1, Pop2, and Pop3) were tested for resistance to bacterial streak in three Louisiana environments with two to three replications per environment from 1991 to 1994. Variation due to genotype x environment (G x E) interaction occurred in each of the populations and was one-fourth to one-half the magnitude of error variance. Heritability of resistance to bacterial streak was relatively low and ranged from 0.12 to 0.70 (average 0.31) with parent-offspring regression and from 0.18 to 0.40 with variance components (average 0.36). Heritability increased by 0.22, 0.29, and 0.29 for Pop1, Pop2, and Pop3, respectively, with means of two replications and two environments. Non-normal distributions in two of the three populations may have inflated estimates of heritability. Across populations, four lines were resistant in all three environments and 12 lines were resistant in two of three environments. Because of GxE interaction, testing should be conducted with at least two replications in two environments under high disease pressure. Such a testing program should be effective in selecting wheat lines resistant to bacterial streak.

Smooth bromegrass (Bromus inermis Leysser) germplasm PL-BDR1 and two seed increase generations derived from it are highly resistant to brown leaf spot caused by Pyrenophora bromi (Died.) Drechs. [Drechslera bromi (Died.) Shoemaker, conidial state = Helminthosporium bromi Died.)]. Lesions are about one-half the width and one-tenth the area of spots on susceptible cultivars. Physiological or anatomical mechanisms of resistance have not been identified, but they could have a hearing on stability of resistance and on forage quality components. This study was conducted to determine whether certain resistance mechanisms identified in other leaf spot diseases of grasses operate in PL-BDR1 germplasm. The three resistant generations were compared with susceptible cultivars Belmont, Radisson, and Saratoga for fungal penetration, halo formation, and leaf vein architecture. Susceptible leaves supported higher numbers of penetration attempts and successful penetrations. No effect of plant line was found for appositionai wall formation (=papilla formation), initial colonization rate, distance between parallel veins, proportion of large vascular bundles, or girdering of vascular bundles. Resistant lines had wider vascular bundles than susceptible cultivars indicating a possible role for strength of the vascular framework in restricting lateral spread. Extensive cell necrosis and chlorotic halo formation in susceptible cultivars indicated possible involvement of a fungal phytotoxin. Resistant lines had few halos, and reduced sensitivity to toxins may be involved in resistance of PL-BDR1 to brown leaf spot.

The replicase enzymes of tobacco inhibit the transcription or movement of the cucumber mosaic viruses (CMV) by directly acting on the viral RNA. The binding of replicase to an inactive 2a transgene protein, encoded by the CMV-RNA2 gene, inhibits the formation of a functional complex. In the absence of a functional complex, the CMV is unable to replicate. Replicase also confers resistance by inhibiting the movement of CMV. The accumulation and transcription of viral RNA is unaffected.

The phosphorylation cascade induced by phosphorylation of the tomato Pto-interacting 1 (Pti1) protein kinase by Pto induces the hypersensitive response (HR). Pti1 expressed in tobacco plants increases HR in response to an avirulence gene. Pti1 is a serine/threonine kinase and acts downstream of Pto. It is unable to phosphorylate Pto or Fen, a related kinase. The HR confers gene-for-gene disease resistance to the plants.

A study was conducted to examine RPG1 and RPM1, two disease resistance genes in soybean and Arabidopsis. These genes confer resistance to infections caused by Pseudomonas syringiae strains which express the avirulence gene avrB. The results showed that alleles, or closely linked genes, exist at the RPG1 locus in soybean that are specific for either avrB or avrPrm1. It is suggested that the alleles can distinguish between these two avirulence genes.

In recent years, it has become apparent that salicylic acid (SA) plays an important role in plant defense responses to pathogen attack. Previous studies have suggested that one of SA's mechanisms of action is the inhibition of catalase, resulting in elevated levels of [H.sub.2][O.sub.2], which activate defense-related genes. Here we demonstrate that SA also inhibits ascorbate peroxidase (APX), the other key enzyme for scavenging [H.sub.2][O.sub.2]. The synthetic inducer of defense responses, 2,6-dichloroisonicotinic acid (INA), was also found to be an effective inhibitor of APX. In the presence of 750 [mu]M ascorbic acid (AsA), substrate-dependent [IC.sub.50] values of 78 [mu]M and 95 [mu]M were obtained for SA and INA, respectively. Furthermore, the ability of SA analogues to block APX activity correlated with their ability to induce defense-related genes in tobacco and enhance resistance to tobacco mosaic virus. Inhibition of APX by SA appears to be reversible, thus differing from the time-dependent, irreversible inactivation by suicide substrates such as p-aminophenol. In contrast to APX, the guaiacol-utilizing peroxidases, which participate in the synthesis and crosslinking of cell wall components as part of the defense response, are not inhibited by SA or INA. The inhibition of both catalase and APX, but not guaiacol peroxidases, supports the hypothesis that SA-induced defense responses are mediated, in part, through elevated [H.sub.2][O.sub.2] levels or coupled perturbations of the cellular redox state.

A mutant strain nim1 (non-inducible immunity phenotype) of Arabidopsis is unable to induce the expression of the systemic acquired resistance (SAR) genes in response to salicyclic acid (SA) or 2,6-dichloroisonicotinic acid. However the increase in the amount of SA which is an endogenous signal for SAR is seen in nim1 which also support the growth of normally incompatible fungal pathogens. Nim1 gene probably encodes a substance required for signal transduction in the pathway which controls the expression of the SAR genes and confers resistance to the plant.

The locus NDR1 (non-race-specific disease resistance) present in Arabidopsis thaliana is necessary for the disease resistance of the plant to the bacteria, Pseudomonas syringae pv. tomato strain DC3000 containing non virulent genes and the fungus Peronospora parasitica. A mutant Arabidopsis strain ndr1-1 in which the mutation segregates as a single recessive gene on chromosome III is susceptible to these pathogens. NDR1 is necessary for the recognition of an avirulent pathogen and the resistance to these unrelated pathogens involves a common step in the molecular pathway.

Cloning of the disease-resistance gene RPS2 of Arabidopsis thaliana makes it possible to use it as a model host to study the genetic aspects of plant defense mechanisms to microbial pathogens. RPS2 corresponds to the avirulence gene avrRpt2 in a gene-for-gene relationship, is similar to the tobacco N resistance gene and encodes a 105-kDa protein comprising a leucine zipper, a nucleotide binding site and 14 imperfect leucine-rich repeats.

Salicylic acid (SA) plays a major role in inducing systemic acquired resistance, a natural plant defense mechanism against pathogen attack. This is evident in the high concentration levels of SA in a tobacco plant infected with tobacco mosaic virus. Besides this, SA assists in developing genetic resistance to diseases. H2O2, unlike SA, apparently does not induce systemic acquired resistance, even though SA inhibition of catalase gives rise to accumulation of H2O2.

The structure and evolution of two chromosome sites of flax (Linum usitatissimum) are different, although the rust resistance genes against pathogens at each site have sequence similarities. While the L locus is simple and has a single gene with 13 alleles, the M locus is complex and contains a tandem array of genes of similar sequence.

Resistance to plant diseases may be guided by gene-for-gene interaction in which a single resistance gene (Pto) responds to the expression of a specific avirulence gene in the pathogen. In a tomato plant affected by bacterial speck disease, the Pto gene is associated with a hypersensitive response upon exposure to the organophosphorous insecticide fenthion. The Pto gene and fenthion-sensitivity gene Fen encode similar protein kinases indicating that both participate in signal transduction involved in disease resistance.

The hypersensitive response, product of an interaction between resistance genes and a pathogen avirulence gene product, is a defense mechanism in plants to combat pathogen invasions. In tobacco plants afflicted by the mosaic virus, the resistance gene (N) functions in a signal transduction pathway by stimulating rapid defense responses. A sequence analysis of the N gene reveals that it encodes a protein with an amino-terminal domain.

The plant-insect interaction benefits plants as parasitic and predatory insects are natural enemies of herbivores. Parasitoids eliminate herbivores that attack the plants. A herbivore-induced emission of volatile from plants sends signals to these insects. Emission of odors is well timed and emitted within hours of herbivore attack. They are mostly produced during daytime, when parasitoids are foraging. Volatile signals are clear, large in number and can be distiguished from background odors, but these signals are not specific when various herbivores attack the same plant.

Grand fir (Abies grandis) saplings and cell cultures can be useful in understanding the regulation of defensive oleoresinosis in conifers. The chemical ecological relationship between conifers and bark beetles may cause injury and oleoresin biosynthesis can be useful to improve tree resistance. Studies with grand fir proved more useful than with pine or spruce.

The resultant H2O2 from an oxidative reaction to an avirulent pathogen strain plays an essential role in the formation of a localized hypersensitive response. This hypersensitive response produces many defenses including cell wall formation, lytic enzymes and the localized host cell death that inhibits the spread of infection. An integrated model of the hypersensitive response to an avirulent pathogen attack can be developed.

Plant cell walls have regulatory molecules, oligogalacturonides (OGAs), that stimulate defense gene expression during the disease process. In vitro, the phosphorylation of plant protein 34 is stimulated by OGAs of 13 to 26 residues long, whereas in vivo, fragments of only 10 to 15 residues long stimulate defense responses. A damaged cell wall, however, can allow access to larger fragments.

The elicitor/suspension-cultured parsley cell system is a good model for studying elicitor recognition, signal transduction and defense gene activation. Elicitor binding by a receptor in the plasma membrane causes H2O2 cell responses, which are followed by transient changes in phosphorylation of proteins and activation of defense genes. With some limitations, each individual defense response was seen to be closely mimicked in elicitor/culture parsley cells, thus upholding the validity of the system.