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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.