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Theory predicts that bottom-up ecological forces can affect community dynamics, but whether this extends to the effects of heritable plant variation on tritrophic communities is poorly understood. In a field experiment, I contrasted the effects of plant genotype (28 genotypes; 1064 plants), aphid density, and the presence/absence of mutualistic ants in affecting the per capita population growth of a specialist aphid herbivore, as well as the effects of plant genotype on the third trophic level. Plant genotype strongly affected aphid population growth rate, explaining 29% of the total variation in growth rate, whereas aphid density and ant-aphid interactions explained substantially less variation (

Agrobacterium radiobacter K84, used worldwide to biocontrol crown gall disease caused by Agrobacterium tumefaciens, produces an antiagrobacterial compound called agrocin 84. We report the nucleotide sequence of pAgK84, a 44.42-kb plasmid coding for production of this disubstituted adenine nucleotide antibiotic. pAgK84 encodes 36 ORFs, 17 of which (agn) code for synthesis of or immunity to agrocin 84. Two genes, agnB2 and agnA, encode aminoacyl tRNA synthetase homologues. We have shown that the toxic moiety of agrocin 84 inhibits cellular leucyl-tRNA synthetases and AgnB2, which confers immunity to the antibiotic, is a resistant form of this enzyme. AgnA, a truncated homologue of asparaginyl tRNA synthetase could catalyze the phosphoramidate bond between a precursor of the methyl pentanamide side group and the nucleotide. We propose previously undescribed chemistry, catalyzed by AgnB1, to generate the precursor necessary for this phosphoramidate linkage. AgnC7 is related to ribonucleotide reductases and could generate the 3'-deoxyarabinose moiety of the nucleoside. Bioinformatics suggest that agnC3, agnC4, and agnC6 contribute to maturation of the methyl pentanamide, whereas agnC2 may produce the glucofuranose side group bound to the adenine ring. AgnG is related to bacterial exporters. An agnG mutant accumulated agrocin 84 intracellularly but did not export the antibiotic, pAgK84 is transmissible and encodes genes for conjugative DNA processing but lacks a type IV secretion system, suggesting that pAgK84 transfers by mobilization. By sequence analysis, the deletion engineered into pAgK1026 removed the oriT and essential tra genes, confirming the enhanced environmental safety of this modified form of pAgK84. Agrobacterium radiobacter | biological control | pAgK84

Pathogens can be an important selective agent in plant evolution because they can severely reduce plant fitness and growth. However, the role of pathogen selection on plant evolution depends on the extent of genetic variation for resistance traits and their covariance with host fitness. Although it is usually assumed that resistance traits will covary with plant fitness, this assumption has not been tested rigorously in plant-pathogen interactions. Many plant species are tolerant to herbivores, decoupling the relationship between resistance and fitness. Tolerance to pathogens can reduce selection for resistance and alter the effect of pathogens on plant evolution. In this study, we measured three components of Arabidopsis thaliana resistance (pathogen growth, disease symptoms, and host fitness) to the bacteria Pseudomonas syringae and investigated their covariation to determine the relative importance of resistance and tolerance. We observed extensive quantitative variation in the severity of disease symptoms, the bacterial population size, and the effect of infection on host fitness among 19 accessions of A. thaliana infected with P. syringae. The severity of disease symptoms was strongly and positively correlated with bacterial population size. Although the average fitness of infected plants was smaller than noninfected plants, we found no correlation between the bacterial growth or symptoms expressed by different accessions of A. thaliana and their relative fitness after infection. These results indicate that the accessions studied vary in tolerance to P. syringae, reducing the strength of selection on resistance traits, and that symptoms and bacterial growth are not good predictors of host fitness.

Homologues of the yeast ubiquitin ligase-associated protein SGT1 are required for disease resistance in plants mediated by nucleotide-binding site/leucine-rich repeat (NBS-LRR) proteins. Here, by silencing SGT1 in Nicotiana benthamiana, we extend these findings and demonstrate that SGT1 has an unexpectedly general role in disease resistance. It is required for resistance responses mediated by NBS-LRR and other R proteins in which pathogen-derived elicitors are recognized either inside or outside the host plant cell. A requirement also exists for SGT1 in nonhost resistance in which all known members of a host species are resistant against every characterized isolate of a pathogen. Our findings show that silencing SGT1 affects diverse types of disease resistance in plants and support the idea that R protein-mediated and nonhost resistance may involve similar mechanisms.

In an experiment that directly manipulated grassland plant species richness and composition, decreased plant species richness ('diversity') increased pathogen load (the percentage of leaf area infected by species-specific foliar pathogens across the plant community) in 1998. Pathogen load was almost three times greater in the average monoculture than in the average plot planted with 24 grassland plant species, an approximately natural diversity. Eleven individual diseases increased in severity (percentage of leaf area infected by a single disease) at lower plant species richness, and severity of only one disease was positively correlated with diversity. For 10 of the 11 diseases whose severity was negatively related to diversity, disease severity was positively correlated with host abundance, and in six of these cases, species diversity had no effect on disease severity after controlling for the effects of host abundance. These results suggest that increased abundances of individual host species at lower species diversity increased disease transmission and severity. In 1996 and 1997, similar results for a smaller number of diseases sampled were found in this experiment and another similar one. Although the effect of diversity on disease was highly significant, considerable variance in pathogen load remained among plots of a given diversity level. Much of this residual variance was explained by community characteristics that were a function of the species composition of the communities (the identity of species present vs. those lost). Specifically, communities that lost less disease-prone species had higher pathogen loads; this effect explained more variance in pathogen load than,did diversity. Also, communities that lost the species dominant at high diversity had higher pathogen loads, presumably because relaxed competition allowed greater increases in host abundances, but this effect was weak. Among plant species, disease proneness appeared to be determined more by regional than local processes, because it was better correlated with frequency of the plant species' populations across the region than with local abundance or frequency across the state. In total, our results support the hypothesis that decreased species diversity will increase foliar pathogen load if this increases host abundance and, therefore, disease transmission. Additionally, changes in community characteristics determined by species composition will strongly influence pathogen load. Key words: biodiversity and ecosystem functioning; functional composition; fungal pathogens; global change; habitat simplification; host density; macroecology; parasites; plant community; plant pathogens; polyculture vs. monoculture; species richness.

The mosquitocidal activity of Bacillus sphaericus is because of a binary toxin (Bin), which binds to Culex pipiens maltase 1 (Cpm1), an [alpha]-glucosidase present in the midgut of Culex pipiens larvae. In this work, we studied the molecular basis of the resistance to Bin developed by a strain (GEO) of C. pipiens. Immunohistochemical and in situ hybridization experiments showed that Cpm1 was undetectable in the midgut of GEO larvae, although the gene was correctly transcribed. The sequence of the [cpm1.sub.GEO] cDNA differs from the sequence we previously reported for a susceptible strain ([cpm1.sub.IP]) by seven mutations: six missense mutations and a mutation leading to the premature termination of translation. When produced in insect cells, [Cpm1.sub.IP] was attached to the membrane by a glycosylphosphatidylinositol (GPI). In contrast, the premature termination of translation of [Cpm1.sub.GEO] resulted in the targeting of the protein to the extracellular compartment because of truncation of the GPI-anchoring site. The interaction between Bin and [Cpm1.sub.GEO] and the enzyme activity of the receptor were not affected. Thus, Bin is not toxic to GEO larvae because it cannot interact with the midgut cell membrane, even though its receptor site is unaffected. This mechanism contrasts with other known resistance mechanisms in which point mutations decrease the affinity of binding between the receptor and the toxin.

To identify Arabidopsis mutants that constitutively express systemic acquired resistance (SAR), we constructed reporter lines expressing the firefly luciferase gene under the control of the SAR-inducible PR-1 promoter (PR-1/luc). After EMS mutagenesis of a well-characterized transgenic line, we screened 250,000 [M.sub.2] plants for constitutive expression of the reporter gene in vivo. From a mutant collection containing several hundred putative mutants, we concentrated on 16 mutants lacking spontaneous hypersensitive response (HR) cell death. We mapped 4 of these constitutive immunity (cim) mutants to chromosome arms. Constitutive expression' of disease resistance was established by analyzing responses to virulent Peronospora parasitica and Pseudomonas syringae strains, by RNA blot analysis for endogenous marker genes, and by determination of salicylic acid levels in the mutants. The variety of the cim phenotypes allowed us to define distinct steps in both the canonical SAR signaling pathway and a separate pathway for resistance to Erysiphe cichoracearum, active in only a subset of the mutants.

The resistance of rice to its bacterial blight pathogen Xanthomonas oryzae pv. oryzae (Xoo) has both qualitative and quantitative components that were investigated using three near-isogenic line sets for four resistance (R) genes (Xa4, xa5, xa13, and Xa21) and 12 Xoo races. Our results indicate that these two resistance components of rice plants were associated with the properties of the R genes. The qualitative component of the R genes was reflected by their large effects against corresponding avirulent Xoo races. The quantitative component of the R genes was their residual effects against corresponding virulent races and their epistatic effects, which together could lead to high-level resistance in a race-specific manner. Our results revealed important differences between the different types of R genes. Two R genes, Xa4 and Xa21, showed complete dominance against the avirulent Xoo races and had large residual effects against virulent ones. They acted independently and cumulatively, suggesting they are involved in different pathways of the rice defensive system. The third R gene, xa5, showed partial dominance or additivity to the avirulent Xoo races and had relatively small but significant residual effects against the virulent races. In contrast, xa13 was completely recessive, had no residual effects against the virulent races, and showed more pronounced race specificity. There was a strong interaction leading to increased resistance between xa13 and xa5 and between either of them and Xa4 or Xa21, suggesting their regulatory roles in the rice defensive pathway(s). Our results indicated that high-level and durable resistance to Xoo should be more efficiently achieved by pyramiding different types of R genes.

Genetic variability of Scots pine (Pinus sylvestris L.) for twist rust susceptibility and prospects for genetic improvement of the species have been studied following artificial inoculation of 1-year-old seedlings in greenhouses. Wind-pollinated progenies, factorial and incomplete diallele mating designs were used to compare two natural populations of Scots pine in France and in Poland. Differences between the two natural populations in response to twist rust are apparently the result of local simultaneous adaptation for climatic conditions and pathogen pressure. Genetic improvements for resistance could be achieved quickly through intrapopulation mass or backward selection based on wind-pollinated progeny tests.

Research reveals that plant disease resistance is mediated by MAP kinase 4 (MPK4) activity and its inactivation by transposons result in the development of systemic acquired resistance, elevated salicylic acid levels, and resistance to virulent pathogens.

A new study investigates the inheritance of resistance to the crown rust fungus of smooth bromegrass.

Plant disease epidemics resulting from introductions of exotic fungal plant pathogens are a well known phenomenon. An associated risk - that accelerated pathogen evolution may be occurring as a consequence of genetic exchange between introduced, or introduced and resident, fungal pathogens - is largely unrecognized. This is, in part, because examples of natural, interspecific hybridization in fungi are very rare. Potential evolutionary developments range from the acquisition of new host specificities to emergence of entirely new pathogen taxa. We present evidence from cytological behavior, additive nucleotide bases in repetitive internal transcribed spacer regions of the rRNA-encoding DNA (rDNA), and amplified fragment length polymorphisms of total DNA that a new, aggressive Phytophthora pathogen of alder trees in Europe comprises a range of heteroploid-interspecific hybrids involving a Phytophthora cambivora-like species and an unknown taxon similar to Phytophthora fragariae. The hybrids' marked developmental instabilities, unusual morphological variability, and evidence for recombination in their internal transcribed spacer profiles indicates that they are of recent origin and that their evolution is continuing. The likelihood of such evolutionary events may be increasing as world trade in plants intensifies. However, routine diagnostic procedures currently in use are insufficiently sensitive to allow their detection.

The [Ca.sup.2+] signal is essential for the activation of plant defense responses, but downstream components of the signaling pathway are still poorly defined. Here we demonstrate that specific calmodulin (CAM) isoforms are activated by infection or pathogen-derived elicitors and participate in [Ca.sup.2+]-mediated induction of plant disease resistance responses. Soybean CaM (SCaM)-4 and SCaM-5 genes, which encode for divergent CaM isoforms, were induced within 30 rain by a fungal elicitor or pathogen, whereas other SCaM genes encoding highly conserved CaM isoforms did not show such response. This pathogen-triggered induction of these genes specifically depended on the increase of intracellular [Ca.sup.2+] level. Constitutive expression of SCaM-4 and SCaM-5 in transgenic tobacco plants triggered spontaneous induction of lesions and induces an array of systemic acquired resistance (SAR)-associated genes. Surprisingly, these transgenic plants have normal levels of endogenous salicylic acid (SA). Furthermore, coexpression of nahG gene did not block the induction of SAR-associated genes in these transgenic plants, indicating that SA is not involved in the SAR gene induction mediated by SCaM-4 or SCaM-5. The transgenic plants exhibit enhanced resistance to a wide spectrum of virulent and avirulent pathogens, including bacteria, fungi, and virus. These results suggest that specific CaM isoforms are components of a SA.independent signal transduction chain leading to disease resistance.

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 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.

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.

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.

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.

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.

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.