Showing papers on "Plant disease resistance published in 2000"
TL;DR: Using a map-based cloning strategy, the Pi-ta gene, which is linked to the centromere of chromosome 12, was cloned and it was found that no resistance response is induced in transient assays that use a naturally occurring pi-ta– allele differing only by the serine at position 918.
Abstract: The rice blast resistance ( R ) gene Pi-ta mediates gene-for-gene resistance against strains of the fungus Magnaporthe grisea that express avirulent alleles of AVR-Pita . Using a map-based cloning strategy, we cloned Pi-ta , which is linked to the centromere of chromosome 12. Pi-ta encodes a predicted 928‐amino acid cytoplasmic receptor with a centrally localized nucleotide binding site. A single-copy gene, Pi-ta shows low constitutive expression in both resistant and susceptible rice. Susceptible rice varieties contain pi-ta ‐ alleles encoding predicted proteins that share a single amino acid difference relative to the Pi-ta resistance protein: serine instead of alanine at position 918. Transient expression in rice cells of a Pi-ta 1 R gene together with AVR-Pita 1 induces a resistance response. No resistance response is induced in transient assays that use a naturally occurring pi-ta ‐ allele differing only by the serine at position 918. Rice varieties reported to have the linked Pi-ta 2 gene contain Pi-ta plus at least one other R gene, potentially explaining the broadened resistance spectrum of Pi-ta 2 relative to Pi-ta . Molecular cloning of the AVR-Pita and Pi-ta genes will aid in deployment of R genes for effective genetic control of rice blast disease.
642 citations
TL;DR: Pathogenicity of Pgt-Ug99 was studied in seedling tests of available wheats containing Sr31, as well as other stem rust differential lines, and Virulence to the T. ventricosum-derived gene Sr38, which is linked to Lr37 and Yr17 and occurs in cultivars from Australia, the United Kingdom, and the United States, was not known previously.
Abstract: In much of the world, resistance to stem rust in wheat, caused by Puccinia graminis f. sp. tritici, is based at least in part on the gene Sr31. During February 1999, high levels of stem rust infection were observed on entries in wheat (Triticum aestivum) grown in a nursery at Kalengyere Research Station in Uganda. Because several of the rusted entries were known to carry the 1BL-1RS chromosome translocation containing the Sr31, Lr26, and Yr9 genes for rust resistance, virulence to Sr31 was suspected. Urediniospores, collected in bulk from rusted stems of seven entries containing Sr31, were suspended in light mineral oil and sprayed on primary leaves of 7-day-old seedlings of South African wheat cv. Gamtoos (=Veery #3, pedigree: Kvz/Buho‘S’//Kal/BB). Plants were kept overnight at 19 to 21°C in a dew chamber before placement in a greenhouse at 18 to 25°C. After ≈14 days, urediniospores were collected from large, susceptible-type stem rust pustules and subsequently increased on Gamtoos, which served as a sel...
618 citations
TL;DR: Experimental data have shown that the LRR has a role in determination of specificity, and modification experiments, in which R-gene signaling has been dissociated from specificity in constitutive signal mutants, have provided the potential for non-specific resistance to be expressed from pathogen-infection-induced promoters in transgenic plants.
588 citations
TL;DR: It is found that salicylic acid is required for the elevated resistance caused by the dnd1 mutation but that removal of salicyric acid did not completely eliminate the dwarf and loss-of-HR phenotypes of mutant dND1 plants.
Abstract: Gene-for-gene disease resistance typically includes a programmed cell death response known as the hypersensitive response (HR). The Arabidopsis thaliana dnd1 mutant was previously isolated as a line that failed to produce the HR in response to avirulent Pseudomonas syringae pathogens; plants homozygous for the recessive dnd1-1 mutation still carry out effective gene-for-gene resistance. The dnd1-1 mutation also causes constitutive systemic resistance and elevated levels of salicylic acid. In the present study, a positional cloning approach was used to isolate DND1. DND1 encodes the same protein as AtCNGC2, a cyclic nucleotide-gated ion channel of previously unknown organismal function that can allow passage of Ca2+, K+ and other cations [Leng, Q., Mercier, R. W., Yao, W. & Berkowitz, G. A. (1999) Plant Physiol. 121, 753–761]. By using a nahG transgene, we found that salicylic acid is required for the elevated resistance caused by the dnd1 mutation but that removal of salicylic acid did not completely eliminate the dwarf and loss-of-HR phenotypes of mutant dnd1 plants. A stop codon that would severely truncate the DND1 gene product was identified in the dnd1-1 allele. This demonstrates that broad-spectrum disease resistance and inhibition of the HR can be activated in plants by disruption of a cyclic nucleotide-gated ion channel.
533 citations
TL;DR: It is shown that resistance and tolerance can have fundamentally different evolutionary outcomes, even when they have equivalent short‐term benefit for the host, and these observations suggest a new mechanism for the evolution of mutualism from parasitism.
Abstract: Host organisms can respond to the threat of disease either through resistance defenses (which inhibit or limit infection) or through tolerance strategies (which do not limit infection, but reduce or offset its fitness conse- quences). Here we show that resistance and tolerance can have fundamentally different evolutionary outcomes, even when they have equivalent short-term benefit for the host. As a gene conferring disease resistance spreads through a population, the incidence of infection declines, reducing the fitness advantage of carrying the resistance gene. Thus genes conferring complete resistance cannot become fixed (i.e., universal) by selection in a host population, and diseases cannot be eliminated solely by natural selection for host resistance. By contrast, as a gene conferring disease tolerance spreads through a population, disease incidence rises, increasing the evolutionary advantage of carrying the tolerance gene. Therefore, any tolerance gene that can invade a host population will tend to be driven to fixation by selection. As predicted, field studies of diverse plant species infected by rust fungi confirm that resistance traits tend to be polymorphic and tolerance traits tend to be fixed. These observations suggest a new mechanism for the evolution of mutualism from parasitism, and they help to explain the ubiquity of disease.
530 citations
TL;DR: Three major genes (Pi1, Piz-5 and Pita) for blast resistance on chromosomes 11, 6 and 12, respectively, were fine-mapped and closely linked RFLP markers identified and are being deployed into agronomically superior ricevarieties by marker-aided selection (MAS).
Abstract: Three major genes (Pi1, Piz-5 and Pita) for blast resistance on chromosomes 11, 6 and 12, respectively, were fine-mapped and closely linked RFLP markers identified. New markers for Pi1 and Pita were found that were flanking the genes. The three genes were pyramided using RFLP markers. A PCR-based SAP (sequence amplified polymorphism) marker was used to identify Piz-5 in the segregating population. The plants carrying the two- and three-gene combinations that were tested for resistance to leaf blast in the Philippines and India indicated that combinations including Piz-5 have enhanced resistance than when it is present alone. The genes from the pyramided lines are at present being deployed into agronomically superior ricevarieties by marker-aided selection (MAS).
464 citations
TL;DR: It is demonstrated that the alfalfa antifungal peptide (alfAFP) defensin isolated from seeds of Medicago sativa displays strong activity against the agronomically important fungal pathogen Verticillium dahliae.
Abstract: Defensins are small cysteine-rich peptides with antimicrobial activity. We demonstrate that the alfalfa antifungal peptide (alfAFP) defensin isolated from seeds of Medicago sativa displays strong activity against the agronomically important fungal pathogen Verticillium dahliae. Expression of the alfAFP peptide in transgenic potato plants provides robust resistance in the greenhouse. Importantly, this resistance is maintained under field conditions. There have been no previous demonstrations of a single transgene imparting a disease resistance phenotype that is at least equivalent to those achieved through current practices using fumigants.
463 citations
TL;DR: The isolation of the nematode-resistance gene Gpa2 in potato is described, and it is demonstrated that highly homologous resistance genes of a single resistance-gene cluster can confer resistance to distinct pathogen species.
Abstract: The isolation of the nematode-resistance gene Gpa2 in potato is described, and it is demonstrated that highly homologous resistance genes of a single resistance-gene cluster can confer resistance to distinct pathogen species. Molecular analysis of the Gpa2 locus resulted in the identification of an R-gene cluster of four highly homologous genes in a region of approximately 115 kb. At least two of these genes are active: one corresponds to the previously isolated Rx1 gene that confers resistance to potato virus X, while the other corresponds to the Gpa2 gene that confers resistance to the potato cyst nematode Globodera pallida. The proteins encoded by the Gpa2 and the Rx1 genes share an overall homology of over 88% (amino-acid identity) and belong to the leucine-zipper, nucleotide-binding site, leucine-rich repeat (LZ-NBS-LRR)-containing class of plant resistance genes. From the sequence conservation between Gpa2 and Rx1 it is clear that there is a direct evolutionary relationship between the two proteins. Sequence diversity is concentrated in the LRR region and in the C-terminus. The putative effector domains are more conserved suggesting that, at least in this case, nematode and virus resistance cascades could share common components. These findings underline the potential of protein breeding for engineering new resistance specificities against plant pathogens in vitro.
352 citations
TL;DR: It is concluded that sequence exchange occurs repeatedly between genetically unlinked disease resistance genes through a process of gene conversion.
Abstract: Rx2 confers resistance against potato virus X (PVX). To clone Rx2, we developed a system based on Agrobacterium-mediated transient expression of candidate R genes in transgenic tobacco leaves expressing the PVX coat protein elicitor of Rx2-mediated resistance. Using this system, a potato gene eliciting HR specifically in the presence of the elicitor was identified. Based on genetical and functional analysis, it is concluded that the cloned gene is Rx2. The transient expression system is potentially adaptable to cloning of any other resistance gene. The Rx2 locus is on chromosome V of potato and the encoded protein is highly similar to the products of Rx1 and Rxh1 encoded on potato chromosome XII. Rxh1 has been shown elsewhere to encode a potato cyst nematode resistance gene Gpa2. All three proteins are in the leucine zipper-nucleotide binding site-leucine rich repeat class of resistance gene products. Rx1 and Rx2 are functionally identical and are almost identical in the C terminal region consistent with a role of the leucine rich repeats in recognition of the PVX coat protein. In the N terminal, half there are some regions where the Rx1 and Rx2 proteins are more similar to each other than to the Rxh1 protein. However, in other regions these proteins are more similar to Rxh1 than to each other. Based on this mosaic pattern of sequence similarity, we conclude that sequence exchange occurs repeatedly between genetically unlinked disease resistance genes through a process of gene conversion.
319 citations
TL;DR: The integrated molecular marker map of the chickpea genome was established using 130 recombinant inbred lines from a wide cross between a cultivar resistant to fusarium wilt caused by Fusarium oxysporum Schlecht to serve as a basis for marker-assisted selection and map-based cloning of fusaria wilt resistance genes and other agronomically important genes in future.
Abstract: An integrated molecular marker map of the chickpea genome was established using 130 recombinant inbred lines from a wide cross between a cultivar resistant to fusarium wilt caused by Fusarium oxysporum Schlecht. emend. Snyd. &. Hans f. sp. ciceri (Padwick) Snyd & Hans, and an accession of Cicer reticulatum (PI 489777), the wild progenitor of chickpea. A total of 354 markers were mapped on the RILs including 118 STMSs, 96 DAFs, 70 AFLPs, 37 ISSRs, 17 RAPDs, eight isozymes, three cDNAs, two SCARs and three loci that confer resistance against different races of fusarium wilt. At a LOD-score of 4.0, 303 markers cover 2077.9 cM in eight large and eight small linkage groups at an average distance of 6.8 cM between markers. Fifty one markers (14.4%) were unlinked. A clustering of markers in central regions of linkage groups was observed. Markers of the same class, except for ISSR and RAPD markers, tended to generate subclusters. Also, genes for resistance to races 4 and 5 of fusarium wilt map to the same linkage group that includes an STMS and a SCAR marker previously shown to be linked to fusarium wilt race 1, indicating a clustering of several fusarium-wilt resistance genes around this locus. Significant deviation from the expected 1 : 1 segregation ratio was observed for 136 markers (38.4%, P<0.05). Segregation was biased towards the wild progenitor in 68% of the cases. Segregation distortion was similar for all marker types except for ISSRs that showed only 28.5% aberrant segregation. The map is the most extended genetic map of chickpea currently available. It may serve as a basis for marker-assisted selection and map-based cloning of fusarium wilt resistance genes and other agronomically important genes in future.
311 citations
TL;DR: Tobacco is transformed with two bacterial genes coding for enzymes that convert chorismate into SA by a two-step process and the CSA plants showed a resistance to viral and fungal infection resembling SAR in nontransgenic plants.
Abstract: After a hypersensitive response to invading pathogens, plants show elevated accumulation of salicylic acid (SA), induced expression of plant defense genes, and systemic acquired resistance (SAR) to further infection by a broad range of pathogens. There is compelling evidence that SA plays a crucial role in triggering SAR. We have transformed tobacco with two bacterial genes coding for enzymes that convert chorismate into SA by a two-step process. When the two enzymes were targeted to the chloroplasts, the transgenic (CSA, constitutive SA biosynthesis) plants showed a 500- to 1,000-fold increased accumulation of SA and SA glucoside compared to control plants. Defense genes, particularly those encoding acidic pathogenesis-related (PR) proteins, were constitutively expressed in CSA plants. This expression did not affect the plant phenotype, but the CSA plants showed a resistance to viral and fungal infection resembling SAR in nontransgenic plants.
Journal Article•
TL;DR: Gene Yr18, known to be present in Opata, strongly reduced disease response in field trials and was tightly linked with leaf-rust resistance gene Lr34, which was associated with APR.
Abstract: Stripe (yellow) rust, caused by Puccinia striiformis West, is an important constraint to wheat production in cool environments With the purpose of identifying genes for resistance to the disease, a RFLP mapping population of recombinant inbred lines developed from a synthetic [Triticum turgidum L x Aegilops tauschii (Coss) Schmal] x T aestivum L cv 'Opata 85' cross was visually evaluated for seedling infection type in three greenhouse inoculation tests and for adult-plant disease severity in four field tests at Celaya and Toluca, Mexico A previously unidentified gene from Ae tauschii, designated as Yr28, was located on chromosome arm 4DS Although Yr28 strongly influenced seedling resistance, it showed a strong effect in adult plants at only the warmer of the two field sites A second gene showed high environmental sensitivity in seedling tests, with resistance associa0ted with Opata marker alleles near the adult-plant resistance (APR) gene Yr18 on chromosome arm 7DS Gene Yr18, known to be present in Opata, strongly reduced disease response in field trials and was tightly linked with leaf-rust resistance gene Lr34 Three other regions from Opata on chromosome arms 3BS, 3DS, and 5DS were also associated with APR
TL;DR: While the taxonomic specificity of host R genes may be evolving rapidly, general functions of R alleles may be conserved at homologous loci in related plant genera.
Abstract: Genomic positions of phenotypically defined disease resistance genes (R genes) and R gene homologues were analyzed in three solanaceous crop genera, Lycopersicon (tomato), Solanum (potato), and Capsicum (pepper). R genes occurred at corresponding positions in two or more genomes more frequently than expected by chance; however, in only two cases, both involving Phytophthora spp., did genes at corresponding positions have specificity for closely related pathogen taxa. In contrast, resistances to Globodera spp., potato virus Y, tobacco mosaic virus, and tomato spotted wilt virus were mapped in two or more genera and did not occur in corresponding positions. Without exception, pepper homologues of the cloned R genes Sw-5, N, Pto, Prf, and I2 were found in syntenous positions in other solanaceous genomes and in some cases also mapped to additional positions near phenotypically defined solanaceous R genes. This detailed analysis and synthesis of all available data for solanaceous R genes suggests a working hypothesis regarding the evolution of R genes. Specifically, while the taxonomic specificity of host R genes may be evolving rapidly, general functions of R alleles (e.g., initiation of resistance response) may be conserved at homologous loci in related plant genera.
TL;DR: Evidence for positive selection in the LRR domain for amino acid diversification outside the core conserved beta-strand/beta-turn motif is found, suggesting that more of the L RR structure is available for interaction with target molecules than has previously been reported for other R gene products.
Abstract: Disease resistance (R) genes are found in plants as either simple (single allelic series) loci, or more frequently as complex loci of tandemly repeated genes. These different loci are likely to be under similar evolutionary forces from pathogens, but the contrast between them suggests important differences in mechanisms associated with DNA structure and recombination that generate and maintain R gene diversity. The RPP13 locus in Arabidopsis represents an important paradigm for studying the evolution of an R gene at a simple locus. The RPP13 allele from the accession Nd-1, designated RPP13-Nd, confers resistance to five different isolates of the biotrophic oomycete, Peronospora parasitica (causal agent of downy mildew), and encodes an NBS-LRR type R protein with a putative amino-terminal leucine zipper. The RPP13-Rld allele, cloned from the accession Rld-2, encodes a different specificity. Comparison of three RPP13 alleles revealed a high rate of amino acid divergence within the LRR domain, less than 80% identity overall, compared to the remainder of the protein (> 95% identity). We also found evidence for positive selection in the LRR domain for amino acid diversification outside the core conserved beta-strand/beta-turn motif, suggesting that more of the LRR structure is available for interaction with target molecules than has previously been reported for other R gene products. Furthermore, an amino acid sequence (LLRVLDL) identical in an LRR among RPP13 alleles is conserved in other LZ NBS-LRR type R proteins, suggesting functional significance.
TL;DR: A synthetic gene encoding a N terminus-modified, cecropin–melittin cationic peptide chimera, with broad-spectrum antimicrobial activity, was introduced into two potato cultivars, Desiree and Russet Burbank, causing a striking lesion-mimic phenotype during leaf and tuber development, indicating its utility may be cultivar specific.
Abstract: Here we describe a strategy for engineering transgenic plants with broad-spectrum resistance to bacterial and fungal phytopathogens. We expressed a synthetic gene encoding a N terminus-modified, cecropin-melittin cationic peptide chimera (MsrA1), with broad-spectrum antimicrobial activity. The synthetic gene was introduced into two potato (Solanum tuberosum L.) cultivars, Desiree and Russet Burbank, stable incorporation was confirmed by PCR and DNA sequencing, and expression confirmed by reverse transcription (RT)-PCR and recovery of the biologically active peptide. The morphology and yield of transgenic Desiree plants and tubers was unaffected. Highly stringent challenges with bacterial or fungal phytopathogens demonstrated powerful resistance. Tubers retained their resistance to infectious challenge for more than a year, and did not appear to be harmful when fed to mice. Expression of msrA1 in the cultivar Russet Burbank caused a striking lesion-mimic phenotype during leaf and tuber development, indicating its utility may be cultivar specific. Given the ubiquity of antimicrobial cationic peptides as well as their inherent capacity for recombinant and combinatorial variants, this approach may potentially be used to engineer a range of disease-resistant plants.
TL;DR: The results suggest that some lesion mimic mutations in rice may be involved in disease resistance, and cloning of these genes may provide a clue to developing broad-spectrum resistance to diverse pathogens.
Abstract: Many plant mutants develop spontaneous lesions that resemble disease symptoms in the absence of pathogen attack. In several pathosystems, lesion mimic mutations have been shown to be involved in programmed cell death, which in some instances leads to enhanced disease resistance to multiple pathogens. We investigated the relationship between spontaneous cell death and disease resistance in rice with nine mutants with a range of lesion mimic phenotypes. All nine mutations are controlled by recessive genes and some of these mutants have stunted growth and other abnormal characteristics. The lesion mimics that appeared on the leaves of these mutants were caused by cell death as measured by trypan blue staining. Activation of six defense-related genes was observed in most of the mutants when the mimic lesions developed. Four mutants exhibited significant enhanced resistance to rice blast. One of the mutants, spl11, confers non-race-specific resistance not only to blast but also to bacterial blight. The level of resistance in the spl11 mutant to the two pathogens correlates with the defense-related gene expression and lesion development on the leaves. The results suggest that some lesion mimic mutations in rice may be involved in disease resistance, and cloning of these genes may provide a clue to developing broad-spectrum resistance to diverse pathogens.
TL;DR: Results indicate that resistance mediated via LZ-NBS/LRR R genes is functional and Surprisingly, only eds14 and eds16 were more susceptible to Erysiphe cichoracearum.
Abstract: To identify components of the defense response that limit growth of a biotrophic fungal pathogen, we isolated Arabidopsis mutants with enhanced disease susceptibility to Erysiphe orontii. Our initial characterization focused on three mutants, eds14, eds15, and eds16. None of these is considerably more susceptible to a virulent strain of the bacterial pathogen Pseudomonas syringae pv. maculicola (Psm). All three mutants develop a hypersensitive response when infiltrated with Psm expressing the avirulence gene avrRpt2, which activates resistance via the LZ-NBS/LRR resistance protein encoded by RPS2. The growth of Psm(avrRpt2), while somewhat greater in the mutants than in the wild type, is less than growth of the isogenic virulent strain. These results indicate that resistance mediated via LZ-NBS/LRR R genes is functional. Analysis of the growth of avirulent Peronospora parasitica strains showed that the resistance pathway utilized by TIR-NBS/LRR R genes is also operative in all three mutants. Surprisingly, only eds14 and eds16 were more susceptible to Erysiphe cichoracearum. Analysis of the expression profiles of PR-1, BGL2, PR-5 and PDF1.2 in eds14, eds15, and eds16 revealed differences from the wild type for all the lines. In contrast, these mutants were not significantly different from wild type in the deposition of callose at sites of E. orontii penetration. All three mutants have reduced levels of salicylic acid after infection. eds16 was mapped to the lower arm of chromosome I and found by complementation tests to be allelic to the salicylic acid-deficient mutant sid2.
TL;DR: Evaluated the cost in pathogenic fitness (aggressiveness and persistence) associated with adaptation of Xoo to virulence on near-isogenic rice lines with single R genes (Xa7, Xa10, and Xa4) at two field sites endemic for bacterial blight to support the prediction that Xa7 would be a durable R gene because of a fitness penalty in Xooassociated with adaptation to Xa 7.
Abstract: Durability of plant disease resistance (R) genes may be predicted if the cost of pathogen adaptation to overcome resistance is understood. Adaptation of the bacterial blight pathogen, Xanthomonas oryzae pv. oryzae (Xoo), to virulence in rice is the result of the loss of pathogen avirulence gene function, but little is known about its effect on aggressiveness under field conditions. We evaluated the cost in pathogenic fitness (aggressiveness and persistence) associated with adaptation of Xoo to virulence on near-isogenic rice lines with single R genes (Xa7, Xa10, and Xa4) at two field sites endemic for bacterial blight. Disease severity was high in all 3 years on all lines except the line with Xa7. Of two Xoo lineages (groups of strains inferred to be clonally related based on DNA fingerprinting) detected, one, lineage C, dominated the pathogen population at both sites. All Xoo strains were virulent to Xa4, whereas only lineage C strains were virulent to Xa10. Only a few strains of lineage C were virulent to Xa7. Adaptation to virulence on Xa7 occurred through at least four different pathways and was associated with a reduction in aggressiveness. Loss of avirulence and reduced aggressiveness were associated with mutations at the 3′ terminus of the avrXa7 allele. Strains most aggressive to Xa7 were not detected after the second year, suggesting they were less persistent than less aggressive strains. These experiments support the prediction that Xa7 would be a durable R gene because of a fitness penalty in Xoo associated with adaptation to Xa7.
TL;DR: The results demonstrate the usefulness of MAS in gene pyramiding for BB resistance, particularly for recessive genes, such as xa5 and xa13, that are difficult to select through conventional breeding in the presence of a dominant gene such as Xa21.
Abstract: IR65598-112 and the two sister lines IR65600-42 and IR65600-96 are promising new plant type (NPT) rice lines with high yield potential. However, these lines are susceptible to bacterial blight caused by Xanthomonas oryzae pv. oryzae (Xoo). To improve the resistance of the three NPT lines to Xoo, three bacterial blight (BB) resistance genes, xa5, xa13, and Xa21, were successfully transferred to the NPT lines via a marker-aided backcrossing procedure. Sequence tagged site (STS) markers for the two resistance genes were developed based on DNA sequences of their linked restriction fragment length polymorphism (RFLP) markers (RG556 and RG207 for xa5 and RG136 for xa13). Marker polymorphism for xa5 was detected after digestion of RG556 polymerase chain reaction (PCR) products with MaeII enzyme and digestion of RG136 PCR product with HinfI enzyme for xa13. The STS marker for Xa21 was designed previously from the sequence of a genomic clone RAPD248. Fifty-nine BC 3 F 2 near-isogenic lines (NILs) in the three NPT backgrounds containing one to three BB resistance genes in various combinations were developed through marker-assisted selection (MAS) for the resistance genes and phenotypic selection for the NPT. The BC 3 F 3 NILs having more than one BB resistance gene showed a wider resistance spectrum and manifested increased levels of resistance to the Xoo races, as compared with those having a single BB resistance gene. Results for two F 2 populations and the progeny testing of their F 3 lines showed that MAS reached an accuracy of 95 and 96% of identifying homozygous resistant plants for xa5 and xa13, respectively. These NPT NILs for BB resistance genes provided valuable materials for breeding and genetic studies of single-gene effects and interaction of several resistance genes. The results demonstrate the usefulness of MAS in gene pyramiding for BB resistance, particularly for recessive genes, such as xa5 and xa13, that are difficult to select through conventional breeding in the presence of a dominant gene such as Xa21.
TL;DR: Transgenic grapevines obtained showed enhanced resistance against powdery mildew caused by Uncinula necator and exhibited slight resistance against Elisinoe ampelina inducing anthracnose, resulting in a reduction in disease lesions.
Abstract: The rice chitinase gene (RCC2), classified as class I chitinase, was introduced into the somatic embryos of grapevine (Vitis vinifera L. cv. Neo Muscut) by Agrobacterium infection. After co-cultivation with Agrobacterium, somatic embryos were transferred onto Murashige and Skoog hormone-free medium supplemented with 50 mg/l kanamycin. Transformed secondary or tertiary embryos were selected, and then more than 20 transgenic plantlets were recovered. Two transformants showed enhanced resistance against powdery mildew caused by Uncinula necator. Few disease symptoms were observed on leaves of these transformants compared with those of the non-transformant, although browning and necrotic symptoms, which seemed to constitute a hypersensitive reaction, were observed. Scanning electron microscopic observation revealed that conidial germination, mycelial growth and conidial formation were suppressed on the leaf surface of the transformant. The transgenic grapevines obtained also exhibited slight resistance against Elisinoe ampelina inducing anthracnose, resulting in a reduction in disease lesions. The relationship between the expression of the foreign chitinase gene and the disease resistance is discussed.
TL;DR: Observations suggest that RPP7 initiates resistance through a novel signaling pathway that functions independently of salicylic acid accumulation or jasmonic acid response components, which is not necessary for resistance mediated by these RPP genes.
Abstract: To better understand the genetic requirements for R gene-dependent defense activation in Arabidopsis, we tested the effect of several defense response mutants on resistance specified by eight RPP genes (for resistance to Peronospora parasitica) expressed in the Col-0 background. In most cases, resistance was not suppressed by a mutation in the SAR regulatory gene NPR1 or by expression of the NahG transgene. Thus, salicylic acid accumulation and NPR1 function are not necessary for resistance mediated by these RPP genes. In addition, resistance conferred by two of these genes, RPP7 and RPP8, was not significantly suppressed by mutations in either EDS1 or NDR1. RPP7 resistance was also not compromised by mutations in EIN2, JAR1 or COI1 which affect ethylene or jasmonic acid signaling. Double mutants were therefore tested. RPP7 and RPP8 were weakly suppressed in an eds1-2/ndr1-1 background, suggesting that these RPP genes operate additively through EDS1, NDR1 and as-yet-undefined signaling components. RPP7 was not compromised in coi1/npr1 or coi1/NahG backgrounds. These observations suggest that RPP7 initiates resistance through a novel signaling pathway that functions independently of salicylic acid accumulation or jasmonic acid response components.
TL;DR: The results demonstrate the utility of FB1 for high-throughput isolation of Arabidopsis defense-related mutants and suggest that pathogen-elicited programmed cell death of host cells may be an important feature of compatible plant–pathogen interactions.
Abstract: Fumonisin B1 (FB1), a programmed cell death–eliciting toxin produced by the necrotrophic fungal plant pathogen Fusarium moniliforme , was used to simulate pathogen infection in Arabidopsis. Plants infiltrated with 10 μM FB1 and seedlings transferred to agar media containing 1 μM FB1 develop lesions reminiscent of the hypersensitive response, including generation of reactive oxygen intermediates, deposition of phenolic compounds and callose, accumulation of phytoalexin, and expression of pathogenesis-related ( PR ) genes. Arabidopsis FB1-resistant ( fbr ) mutants were selected directly by sowing seeds on agar containing 1 μM FB1, on which wild-type seedlings fail to develop. Two mutants chosen for further analyses, fbr1 and fbr2 , had altered PR gene expression in response to FB1. fbr1 and fbr2 do not exhibit differential resistance to the avirulent bacterial pathogen Pseudomonas syringae pv maculicola (ES4326) expressing the avirulence gene avrRpt2 but do display enhanced resistance to a virulent isogenic strain that lacks the avirulence gene. Our results demonstrate the utility of FB1 for high-throughput isolation of Arabidopsis defense-related mutants and suggest that pathogen-elicited programmed cell death of host cells may be an important feature of compatible plant–pathogen interactions.
TL;DR: The multiple functions of avrPphF illustrate how effector proteins from plant pathogens have evolved to be recognized by R gene products and, therefore, be classified as encoded by avirulence genes.
Abstract: The avrPphF gene was cloned from Pseudomonas syringae pathovar phaseolicola (Pph) races 5 and 7, based on its ability to confer avirulence towards bean cultivars carrying the R1 gene for halo-blight resistance, such as Red Mexican. avrPphF comprised two open reading frames, which were both required for function, and was located on a 154 kb plasmid (pAV511) in Pph. Strain RW60 of Pph, lacking pAV511, displayed a loss in virulence to a range of previously susceptible cultivars such as Tendergreen and Canadian Wonder. In Tendergreen virulence was restored to RW60 by avrPphF alone, whereas subcloned avrPphF in the absence of pAV511 greatly accelerated the hypersensitive resistance reaction caused by RW60 in Canadian Wonder. A second gene from pAV511, avrPphC, which controls avirulence to soybean, was found to block the activity of avrPphF in Canadian Wonder, but not in Red Mexican. avrPphF also conferred virulence in soybean. The multiple functions of avrPphF illustrate how effector proteins from plant pathogens have evolved to be recognized by R gene products and, therefore, be classified as encoded by avirulence genes.
TL;DR: The overall similarity between the Sw-5 and Mi proteins of tomato suggests that a shared or comparable signal transduction pathway leads to both virus and nematode resistance in tomato, and supports the hypothesis that Sw- 5 provides resistance via a hypersensitive response.
Abstract: We used a positional cloning approach to isolate the Sw-5 disease resistance locus of tomato. Complementation experiments with overlapping cosmid clones enabled us to demonstrate that Sw-5 is a single gene locus capable of recognizing several tospovirus isolates and species. Analysis of the predicted Sw-5 protein suggests that it is a cytoplasmic protein, with a potential nucleotide binding site (NBS) domain and a C-terminal end consisting of leucine-rich repeats (LRRs). Based on its structural features, Sw-5 belongs to the class of NBS-LRR resistance genes that includes the tomato Mi, 12, and Prf genes; the Arabidopsis RPM1 gene; and the plant potato virus X resistance gene Rx. The overall similarity between the Sw-5 and Mi proteins of tomato suggests that a shared or comparable signal transduction pathway leads to both virus and nematode resistance in tomato. The similarity also supports the hypothesis that Sw-5 provides resistance via a hypersensitive response. Sw-5 is a member of a loosely clustered gene family in the telomeric region of chromosome 9. Members of this family map to other regions of chromosome 9 and also to chromosome 12, where several fungal, virus, and nematode genes have been mapped, suggesting that paralogs of Sw-5 may have evolved to provide different resistance specificities.
TL;DR: Though rice sheath blight resistance may be influenced by morphological traits, such as heading date and plant height, in the present study most detected resistance loci were not linked to the loci for heading date or plant height.
Abstract: Rice sheath blight, caused by Rhizoctonia solani Kuhn, is one of the three major diseases of rice. The present study was conducted with an F2 clonal population of Jasmine 85/Lemont. The F2 population, including 128 clonal families, was inoculated by short toothpicks incubated with a strain, RH-9 of the fungus. Based on field disease evaluations in 2 years and a genetic map with 118 evenly distributed molecular markers, we identified six quantitative trait loci (QTLs) contributing to sheath blight resistance. These QTLs, qSB-2, qSB-3, qSB-7, qSB-9-1, qSB-9-2 and qSB-11, were located on chromosomes 2, 3, 7, 9 and 11, respectively. The respective alleles of qSB-2, qSB-3, qSB-7, and qSB-9-2 from Jasmine 85 could explain 21.2%, 26.5%, 22.2% and 10.1% of the total phenotypic variation, respectively; while the alleles of qSB-9-1 and qSB-11 from Lemont could explain 9.8% and 31.2% of the total phenotypic variation. Of these qSB-2 and qSB-11 could be detected in both years, while remaining loci were detected only in a single year. Furthermore, four QTLs (qHD-2, qHD-3, qHD-5 and qHD-7) controlling heading date and three QTLs (qPH-3, qPH-4 and qPH-11) controlling plant height were also identified. Though rice sheath blight resistance may be influenced by morphological traits, such as heading date and plant height, in the present study most detected resistance loci were not linked to the loci for heading date or plant height.
TL;DR: A reliable test was developed to score partial resistance in aerial organs of the plant (stem, leaf, petiole) under controlled growth chamber conditions and BAT93 was more resistant than JaloEEP558 regardless of the organ or strain tested.
Abstract: Anthracnose, one of the most important diseases of common bean (Phaseolus vulgaris), is caused by the fungus Colletotrichum lindemuthianum. A "candidate gene" approach was used to map anthracnose resistance quantitative trait loci (QTL). Candidate genes included genes for both pathogen recognition (resistance genes and resistance gene analogs [RGAs]) and general plant defense (defense response genes). Two strains of C. lindemuthianum, identified in a world collection of 177 strains, displayed a reproducible and differential aggressiveness toward BAT93 and JaloEEP558, two parental lines of P. vulgaris representing the two major gene pools of this crop. A reliable test was developed to score partial resistance in aerial organs of the plant (stem, leaf, petiole) under controlled growth chamber conditions. BAT93 was more resistant than JaloEEP558 regardless of the organ or strain tested. With a recombinant inbred line (RIL) population derived from a cross between these two parental lines, 10 QTL were located on a genetic map harboring 143 markers, including known defense response genes, anthracnose-specific resistance genes, and RGAs. Eight of the QTL displayed isolate specificity. Two were co-localized with known defense genes (phenylalanine ammonia-lyase and hydroxyproline-rich glycoprotein) and three with anthracnose-specific resistance genes and/or RGAs. Interestingly, two QTL, with different allelic contribution, mapped on linkage group B4 in a 5.0 cM interval containing Andean and Mesoamerican specific resistance genes against C. lindemuthianum and 11 polymorphic fragments revealed with a RGA probe. The possible relationship between genes underlying specific and partial resistance is discussed.
TL;DR: In vitro inoculation of grapevine plantlets induced a significant plant growth promotion which made them more hardy and vigorous when compared to non-inoculated plantlets, and this ability increased upon transplanting.
Abstract: The potential of a plant growth-promoting rhizobacterium, Pseudomonas sp. (strain PsJN), to stimulate the growth and enhancement of the resistance of grapevine (Vitis vinifera L.) transplants to gray mould caused by Botrytis cinerea has been investigated. In vitro inoculation of grapevine plantlets induced a significant plant growth promotion which made them more hardy and vigorous when compared to non-inoculated plantlets. This ability increased upon transplanting. When grown together with B. cinerea, the causal agent of gray mould, significant differences of aggressiveness were observed between the inoculated and non-inoculated plants. The presence of bacteria was accompanied by an induction of plant resistance to the pathogen. The beneficial effect from this plant–microbe association is being postulated.
TL;DR: Sequence-characterized amplified regions (SCARs) were developed, based on nucleotide differences within resistance gene-like fragments isolated from a potato plant carrying the Ryadg gene, which confers extreme resistance to potato Y potyvirus (PVY).
Abstract: Sequence-characterized amplified regions (SCARs) were developed, based on nucleotide differences within resistance gene-like fragments isolated from a potato plant carrying the Ryadg gene, which confers extreme resistance to potato Y potyvirus (PVY). It originates from Solanum tuberosum subsp. andigena, and a susceptible potato plant. SCARs were tested using 103 potato breeding lines and cultivars with diverse genetic backgrounds derived from Europe, North America, and Japan. Two markers showed high accuracy for detection of the Ryadg gene. The SCAR marker RYSC3 was generated only in genotypes carrying Ryadg. The SCAR marker RYSC4 was detected in all genotypes carrying Ryadg but also in four PVY-susceptible genotypes. Neither marker was detected in genotypes carrying other Ry genes originating from different species than S. tuberosum subsp. andigena. Therefore, these SCAR markers should be powerful tools in marker-assisted selection for Ryadg in potato breeding programs, and should also be useful for cloning of the Ryadg gene.
TL;DR: The identification of Rcr3, a tomato gene required specifically for Cf-2-mediated resistance, is reported, suggesting that Avr products interact with host proteins to promote disease, and that R proteins "guard" these host components and initiate Avr-dependent plant defense responses.
Abstract: Genetic analysis of plant-pathogen interactions has demonstrated that resistance to infection is often determined by the interaction of dominant plant resistance (R) genes and dominant pathogen-encoded avirulence (Avr) genes. It was postulated that R genes encode receptors for Avr determinants. A large number of R genes and their cognate Avr genes have now been analyzed at the molecular level. R gene loci are extremely polymorphic, particularly in sequences encoding amino acids of the leucine-rich repeat motif. A major challenge is to determine how Avr perception by R proteins triggers the plant defense response. Mutational analysis has identified several genes required for the function of specific R proteins. Here we report the identification of Rcr3, a tomato gene required specifically for Cf-2-mediated resistance. We propose that Avr products interact with host proteins to promote disease, and that R proteins "guard" these host components and initiate Avr-dependent plant defense responses.