Interfamily Transfer of Dual NB-LRR Genes Confers Resistance to Multiple Pathogens

A major class of disease resistance (R) genes which encode nucleotide binding and leucine rich repeat (NB-LRR) proteins have been used in traditional breeding programs for crop protection. However, it has been difficult to functionally transfer NB-LRR-type R genes in taxonomically distinct families. Here we demonstrate that a pair of Arabidopsis (Brassicaceae) NB-LRR-type R genes, RPS4 and RRS1, properly function in two other Brassicaceae, Brassica rapa and Brassica napus, but also in two Solanaceae, Nicotiana benthamiana and tomato (Solanum lycopersicum). The solanaceous plants transformed with RPS4/RRS1 confer bacterial effector-specific immunity responses. Furthermore, RPS4 and RRS1, which confer resistance to a fungal pathogen Colletotrichum higginsianum in Brassicaceae, also protect against Colletotrichum orbiculare in cucumber (Cucurbitaceae). Importantly, RPS4/RRS1 transgenic plants show no autoimmune phenotypes, indicating that the NB-LRR proteins are tightly regulated. The successful transfer of two R genes at the family level implies that the downstream components of R genes are highly conserved. The functional interfamily transfer of R genes can be a powerful strategy for providing resistance to a broad range of pathogens.     

A dual resistance gene system prevents infection by three distinct pathogens

Colletotrichum higginsianum causes typical anthracnose lesions on the leaves, petioles, and stems of cruciferous plants. Inoculation of Arabidopsis thaliana ecotype Columbia leaves with C. higginsianum results in fungal growth and disease symptoms reminiscent of those induced in other cruciferous plants. We performed map-based cloning and natural variation analysis of 19 A. thaliana ecotypes to identify a dominant resistance locus against C. higginsianum. We found that the A. thaliana RCH2 (for recognition of C. higginsianum) locus encodes two NB-LRR proteins, both of which are required for resistance to C. higginsianum in the A. thaliana ecotype Ws-0. Both proteins are well-characterized R proteins involved in resistance against bacterial pathogens; RRS1 (resistance to Ralstonia solanacearum 1) confers resistance to strain Rs1000 of R. solanacearum and RPS4 to Pseudomonas syringae pv. tomato strain DC3000 expressing avrRps4 (Pst-avrRps4). Furthermore, we found that both RRS1-Ws and RPS4-Ws genes are required for resistance to Pst-avrRps4 and to Rs1002 R. solanacearum. We therefore demonstrate that a pair of neighboring genes, RRS1-Ws and RPS4-Ws, function cooperatively as a dual R-gene system against at least three distinct pathogens.Key words: R gene, RPS4, RRS1, Colletotrichum higginsianum, Pseudomonas syringae, Ralstonia solanacearumPlants are exposed to various types of potentially invasive organisms, including viruses, bacteria, fungi, nematodes and protozoa, but are able to defend themselves by activating multiple defense mechanisms. The gene-for-gene hypothesis¹ provides a mechanism for specific recognition of the pathogen by the plant. This recognition is mediated by direct or indirect interactions between the product of a plant resistance (R) gene and the corresponding effectors encoded by avirulence genes in the pathogen.² Most R-genes encode non-membrane proteins that contain a conserved nucleotide-binding (NB) site and a carboxy-terminal leucine-rich repeat (LRR) domain.The A. thaliana genome contains about 150 genes coding for NB-LRR-containing proteins.³ This is far less than the number of genes that would be required to respond individually and specifically to all of its potential pathogens. However, plants may have been able to limit the number of required NB-LRR-encoding genes if host proteins perceive sets of distinct pathogens.⁴Colletotrichum species cause devastating anthracnose diseases in a large number of agronomically important crops. These diseases can often be controlled by introduction of genetic resistance traits, but the molecular components of resistance remain unknown. Inoculation of A. thaliana ecotype Columbia (Col-0) leaves with Colletotrichum higginsianum results in fungal growth and disease symptoms reminiscent of those induced in other cruciferous plants.^5,6 Inoculation of a large number of ecotypes with isolates of C. higginsianum showed that A. thaliana has at least two dominant resistance gene loci, designated RCH1 and RCH2 (for recognition of C. higginsianum), indicating that A. thaliana resistance to C. higginsianum is controlled by a “gene-for-gene” interaction.⁵ In a previous study, we identified a single putative R locus, RCH1 on the top of chromosome 4, in the C. higginsianum-resistant A. thaliana ecotype Eil-0.⁵In the present study, the locus named RCH2 maps in an extensive cluster of disease-resistance loci known as MRC-J in the A. thaliana ecotype Ws-0. By analyzing natural variations within the MRC-J region, we found that alleles of RRS1 (resistance to Ralstonia solanacearum 1) from susceptible ecotypes contain single nucleotide polymorphisms that may affect the encoded protein. Consistent with this finding, two susceptible mutants, rrs1-1 and rrs1–2, were identified by screening a T-DNA-tagged mutant library for the loss of resistance to C. higginsianum. The screening identified an additional susceptible mutant (rps4-21), which has a 5-bp deletion in the neighboring gene, RPS4-Ws, a well-characterized R gene that provides resistance to Pseudomonas syringae pv. tomato strain DC3000 expressing avrRps4 (Pst-avrRps4). To assess if RRS1-Ws and RPS4-Ws function in concert, we generated an rps4-21/rrs1-1 double mutant by crossing rps4-21 and rrs1-1 mutants. The susceptibility levels of rps4-21/rrs1-1 double mutant to C. higginsianum were similar to that exhibited by the single mutants, suggesting that RRS1-Ws and RPS-4-Ws function cooperatively. We also found that both RRS1 and RPS4 are required for resistance to R. solanacearum and Pst-avrRps4. Thus, these two adjacent R genes confer resistance, in tandem or individually, to three distinct pathogens with very different infection strategies and virulence mechanisms (Fig. 1).Open in a separate windowFigure 1RPS4 and RRS1 function as a dual resistance gene system that prevents infection by three distinct pathogens (Colletotrichum higginsianum, Ralstonia solanacearum and Pseudomonas syringae pv. tomato strain DC3000 expressing avrRps4).Several examples of two NB-LRR genes acting cooperatively to confer resistance against a pathogen have been reported. For example, A. thaliana RPP2A and RPP2B reside adjacently in the RPP2 locus.⁷ Blast resistance in Pikm-containing rice is conferred by a combination of two NB-LRR encoding genes, Pikm1-TS and Pikm2-TS.⁸ Pi5-mediated resistance against rice blast requires two NB-LRR-encoding genes.⁹ It is not known whether these NB-LRR genes function cooperatively or independently. Because of structural similarity with RRS1/RPS4 genes, it is possible that resistance to the pathogens is conferred by cooperation between the two NB-LRR genes.Several reports have shown that a single R gene/locus can confer resistance to multiple pathogens. For instance, tomato Mi mediates resistance against three distinct types of pests, including root-knot nematodes, potato aphids and sweet potato whitefly.¹⁰ In the present study, we suggest that two distinct R-genes located in a conserved head-to-head organization confer resistance to three distinct pathogen species by acting cooperatively.The tandem function of RRS1-Ws and its neighboring gene RPS4-Ws is also supported by the evolutionary conservation of the gene pair. Close homologs of RPS4 are often physically paired with homologs of RRS1 in a head-to-head (inverted) tandem arrangement.¹¹ The evolutionary conservation of homologous gene pairs in a head-to-head arrangement also supports the idea that cooperative function of two R genes could be a common mechanism of defense against pathogens. Since the two open reading frames are only 264 bp apart, the promoter regions of the gene pairs possibly overlap, leading to co-regulation of the genes. The head-to-head configuration may assure balanced levels of the protein pair to meet a strict stoichiometric requirement to act together, possibly in a complex. As a practical application, this finding may provide a new strategy for creating transgenic plants that express R genes from other plants. Introduction of two R genes in a head-to-head orientation may be necessary for effective pathogen resistance.     

A locus conferring resistance to Colletotrichum higginsianum is shared by four geographically distinct Arabidopsis accessions

Colletotrichum higginsianum is a hemibiotrophic fungal pathogen that causes anthracnose disease on Arabidopsis and other crucifer hosts. By exploiting natural variation in Arabidopsis we identified a resistance locus that is shared by four geographically distinct accessions (Ws‐0, Kondara, Gifu‐2 and Can‐0). A combination of quantitative trait loci (QTL) and Mendelian mapping positioned this locus within the major recognition gene complex MRC‐J on chromosome 5 containing the Toll‐interleukin‐1 receptor/nucleotide‐binding site/leucine‐rich repeat (TIR‐NB‐LRR) genes RPS4 and RRS1 that confer dual resistance to C. higginsianum in Ws‐0 ( Narusaka et al., 2009 ). We find that the resistance shared by these diverse Arabidopsis accessions is expressed at an early stage of fungal invasion, at the level of appressorial penetration and establishment of intracellular biotrophic hyphae, and that this determines disease progression. Resistance is not associated with host hypersensitive cell death, an oxidative burst or callose deposition in epidermal cells but requires the defense regulator EDS1, highlighting new functions of TIR‐NB‐LRR genes and EDS1 in limiting early establishment of fungal biotrophy. While the Arabidopsis accession Ler‐0 is fully susceptible to C. higginsianum infection, Col‐0 displays intermediate resistance that also maps to MRC‐J. By analysis of null mutants of RPS4 and RRS1 in Col‐0 we show that these genes, individually, do not contribute strongly to C. higginsianum resistance but are both required for resistance to Pseudomonas syringae bacteria expressing the Type III effector, AvrRps4. We conclude that distinct allelic forms of RPS4 and RRS1 probably cooperate to confer resistance to different pathogens.     

RRS1 and RPS4 provide a dual Resistance-gene system against fungal and bacterial pathogens

Colletotrichum higginsianum is a fungal pathogen that infects a wide variety of cruciferous plants, causing important crop losses. We have used map-based cloning and natural variation analysis of 19 Arabidopsis ecotypes to identify a dominant resistance locus against C. higginsianum . This locus named RCH2 (for recognition of C. higginsianum ) maps in an extensive cluster of disease-resistance loci known as MRC-J in the Arabidopsis ecotype Ws-0. By analyzing natural variations within the MRC-J region, we found that alleles of RRS1 ( resistance to Ralstonia solanacearum 1 ) from susceptible ecotypes contain single nucleotide polymorphisms that may affect the encoded protein. Consistent with this finding, two susceptible mutants, rrs1-1 and rrs1-2 , were identified by screening a T-DNA-tagged mutant library for the loss of resistance to C. higginsianum . The screening identified an additional susceptible mutant ( rps4-21 ) that has a 5-bp deletion in the neighboring gene, RPS4-Ws , which is a well-characterized R gene that provides resistance to Pseudomonas syringae pv. tomato strain DC3000 expressing avrRps4 ( Pst - avrRps4 ). The rps4-21 / rrs1-1 double mutant exhibited similar levels of susceptibility to C. higginsianum as the single mutants. We also found that both RRS1 and RPS4 are required for resistance to R. solanacearum and Pst-avrRps4 . Thus, RPS4-Ws and RRS1-Ws function as a dual resistance gene system that prevents infection by three distinct pathogens.     

Temperature Modulates Plant Defense Responses through NB-LRR Proteins

An elevated growth temperature often inhibits plant defense responses and renders plants more susceptible to pathogens. However, the molecular mechanisms underlying this modulation are unknown. To genetically dissect this regulation, we isolated mutants that retain disease resistance at a higher growth temperature in Arabidopsis. One such heat-stable mutant results from a point mutation in SNC1, a NB-LRR encoding gene similar to disease resistance (R) genes. Similar mutations introduced into a tobacco R gene, N, confer defense responses at elevated temperature. Thus R genes or R-like genes involved in recognition of pathogen effectors are likely the causal temperature-sensitive component in defense responses. This is further supported by snc1 intragenic suppressors that regained temperature sensitivity in defense responses. In addition, the SNC1 and N proteins had a reduction of nuclear accumulation at elevated temperature, which likely contributes to the inhibition of defense responses. These findings identify a plant temperature sensitive component in disease resistance and provide a potential means to generate plants adapting to a broader temperature range.     

Disease resistance in rice and the role of molecular breeding in protecting rice crops against diseases

Rice diseases (bacterial, fungal, or viral) threaten food productivity. Host resistance is the most efficient, environmentally friendly method to cope with such diverse pathogens. Quantitative resistance conferred by quantitative trait loci (QTLs) is a valuable resource for rice disease resistance improvement. Although QTLs confer partial but durable resistance to many pathogen species in different crop plants, the molecular mechanisms of quantitative disease resistance remain mostly unknown. Quantitative resistance and non-host resistance are types of broad-spectrum resistance, which are mediated by resistance (R) genes. Because R genes activate different resistance pathways, investigating the genetic spectrum of resistance may lead to minimal losses from harmful diseases. Genome studies can reveal interactions between different genes and their pathways and provide insight into gene functions. Protein–protein interaction (proteomics) studies using molecular and bioinformatics tools may further enlighten our understanding of resistance phenomena.     

Resistance to Colletotrichum lindemuthianum in Phaseolus vulgaris: a case study for mapping two independent genes

Anthracnose, caused by the hemibiotrophic fungal pathogen Colletotrichum lindemuthianum is a devastating disease of common bean. Resistant cultivars are economical means for defense against this pathogen. In the present study, we mapped resistance specificities against 7 C. lindemuthianum strains of various geographical origins revealing differential reactions on BAT93 and JaloEEP558, two parents of a recombinant inbred lines (RILs) population, of Meso-american and Andean origin, respectively. Six strains revealed the segregation of two independent resistance genes. A specific numerical code calculating the LOD score in the case of two independent segregating genes (i.e. genes with duplicate effects) in a RILs population was developed in order to provide a recombination value (r) between each of the two resistance genes and the tested marker. We mapped two closely linked Andean resistance genes (Co-x, Co-w) at the end of linkage group (LG) B1 and mapped one Meso-american resistance genes (Co-u) at the end of LG B2. We also confirmed the complexity of the previously identified B4 resistance gene cluster, because four of the seven tested strains revealed a resistance specificity near Co-y from JaloEEP558 and two strains identified a resistance specificity near Co-9 from BAT93. Resistance genes found within the same cluster confer resistance to different strains of a single pathogen such as the two anthracnose specificities Co-x and Co-w clustered at the end of LG B1. Clustering of resistance specificities to multiple pathogens such as fungi (Co-u) and viruses (I) was also observed at the end of LG B2.     

Quantitative disease resistance to the bacterial pathogen Xanthomonas campestris involves an Arabidopsis immune receptor pair and a gene of unknown function

Although quantitative disease resistance (QDR) is a durable and broad‐spectrum form of resistance in plants, the identification of the genes underlying QDR is still in its infancy. RKS1 (Resistance related KinaSe1) has been reported recently to confer QDR in Arabidopsis thaliana to most but not all races of the bacterial pathogen Xanthomonas campestris pv. campestris (Xcc). We therefore explored the genetic bases of QDR in A. thaliana to diverse races of X. campestris (Xc). A nested genome‐wide association mapping approach was used to finely map the genomic regions associated with QDR to Xcc12824 (race 2) and XccCFBP6943 (race 6). To identify the gene(s) implicated in QDR, insertional mutants (T‐DNA) were selected for the candidate genes and phenotyped in response to Xc. We identified two major QTLs that confer resistance specifically to Xcc12824 and XccCFBP6943. Although QDR to Xcc12824 is conferred by At5g22540 encoding for a protein of unknown function, QDR to XccCFBP6943 involves the well‐known immune receptor pair RRS1/RPS4. In addition to RKS1, this study reveals that three genes are involved in resistance to Xc with strikingly different ranges of specificity, suggesting that QDR to Xc involves a complex network integrating multiple response pathways triggered by distinct pathogen molecular determinants.     

Identification of a disease resistance locus in Arabidopsis that is functionally homologous to the RPG1 locus of soybean

A new disease resistance locus in Arabidopsis, RPS3 , was identified using a previously cloned avirulence gene from a non- Arabidopsis pathogen. The avrB avirulence gene from the soybean pathogen Pseudomonas syringae pv. glycinea was transferred into a P. syringae pv. tomato strain that is virulent on Arabidopsis , and conversion to avirulence was assayed on Arabidopsis plants. The avrB gene had avirulence activity on most, but not all, Arabidopsis ecotypes. Of 53 ecotypes examined, 45 were resistant to a P. syringae pv. tomato strain carrying avrB , and eight were susceptible. The inheritance of this resistance was examined using crosses between the resistant ecotype Col-0 and the susceptible ecotype Bla-2. In F₂ plants from this cross, the ratio of resistant:susceptible plants was approximately 3:1, indicating that resistance to P. syringae expressing avrB is determined by a single dominant locus in ecotype Col-0, which we have designated RPS3 . Using RFLP analysis, RPS3 was mapped to chromosome 3, adjacent to markers M583 and G4523, and ≤ 1 cM from another disease resistance locus, RPM1 . In soybean, resistance to P. syringae strains that carry avrB is controlled by the locus RPG1 . Thus, RPG1 and RPS3 both confer avrB -specific disease resistance, suggesting that these genes may be homologs.     

Molecular breeding: marker-assisted selection combined with biolistic transformation for blast and bacterial blight resistance in Indica rice (cv. CO39)

Based on blast pathogen population dynamics and lineage exclusion assays, we found that the major blast resistance genes Pi-1 and Piz-5 confer resistance against most Magnaporthe grisea lineages. Near-isogenic rice lines C101LAC and C101A51 carrying these two major genes for blast resistance in the background of a most blast-susceptible genotype were used for developing the pyramids. The closely linked RFLP marker RZ536 and NBS-LRR r10 marker for Pi-1 and a PCR-based SAP marker RG64 for Piz-5 were used to identify the genes in the parents and in marker-assisted breeding of the pyramided populations. To achieve multiple resistance against blast and blight in this cultivar, these blast-resistant pyramids were transformed with the cloned bacterial blight resistance gene Xa21 known to confer resistance to all races of Xanthomonas oryzae pv. oryzae (Xoo). Bioassays with six independent transformants showed that transgenic CO39 plants were resistant to both pathogens, M. grisea and Xoo. We report here the stacking of three major genes (Pi-1 + Piz-5 + Xa21) into rice using two different approaches of molecular breeding: marker-assisted selection (MAS) and genetic transformation.     

Molecular mechanisms involved in bacterial speck disease resistance of tomato

An important recent advance in the field of plant-microbe interactions has been the cloning of genes that confer resistance to specific viruses, bacteria, fungi or nematodes. Disease resistance (R) genes encode proteins with predicted structural motifs consistent with them having roles in signal recognition and transduction. The future challenge is to understand how R gene products specifically perceive defence-eliciting signals from the pathogen and transduce those signals to pathways that lead to the activation of plant defence responses. In tomatoes, the Pto kinase (product of the Pto R gene) confers resistance to strains of the bacterial speck pathogen, Pseudomonas syringae pv. tomato, that carry the corresponding avirulence gene avrPto. Resistance to bacterial speck disease is initiated by a mechanism involving the physical interaction of the Pto kinase and the AvrPto protein. This recognition event initiates signalling events that lead to defence responses including an oxidative burst, the hypersensitive response and expression of pathogenesis-related genes. Pto-interacting (Pti) proteins have been identified that appear to act downstream of the Pto kinase and our current studies are directed at elucidating the roles of these components.     

<Emphasis Type="Italic">STAYGREEN</Emphasis> (<Emphasis Type="Italic">CsSGR</Emphasis>) is a candidate for the anthracnose (<Emphasis Type="Italic">Colletotrichum orbiculare</Emphasis>) resistance locus <Emphasis Type="Italic">cla</Emphasis> in Gy14 cucumber

Key message

Map-based cloning identified a candidate gene for resistance to the anthracnose fungal pathogen Colletotrichum orbiculare in cucumber, which reveals a novel function for the highly conserved STAYGREEN family genes for host disease resistance in plants.

Abstract

Colletotrichum orbiculare is a hemibiotrophic fungal pathogen that causes anthracnose disease in cucumber and other cucurbit crops. No host resistance genes against the anthracnose pathogens have been cloned in crop plants. Here, we reported fine mapping and cloning of a resistance gene to the race 1 anthracnose pathogen in cucumber inbred lines Gy14 and WI 2757. Phenotypic and QTL analysis in multiple populations revealed that a single recessive gene, cla, was underlying anthracnose resistance in both lines, but WI2757 carried an additional minor-effect QTL. Fine mapping using 150 Gy14?×?9930 recombinant inbred lines and 1043 F₂ individuals delimited the cla locus into a 32 kb region in cucumber Chromosome 5 with three predicted genes. Multiple lines of evidence suggested that the cucumber STAYGREEN (CsSGR) gene is a candidate for the anthracnose resistance locus. A single nucleotide mutation in the third exon of CsSGR resulted in the substitution of Glutamine in 9930 to Arginine in Gy14 in CsSGR protein which seems responsible for the differential anthracnose inoculation responses between Gy14 and 9930. Quantitative real-time PCR analysis indicated that CsSGR was significantly upregulated upon anthracnose pathogen inoculation in the susceptible 9930, while its expression was much lower in the resistant Gy14. Investigation of allelic diversities in natural cucumber populations revealed that the resistance allele in almost all improved cultivars or breeding lines of the U.S. origin was derived from PI 197087. This work reveals an unknown function for the highly conserved STAYGREEN (SGR) family genes for host disease resistance in plants.

     

A disease resistance gene in Arabidopsis with specificity for two different pathogen avirulence genes.

The RPS3 and RPM1 disease resistance loci of Arabidopsis confer resistance to Pseudomonas syringae strains that carry the avirulence genes avrB and avrRpm1, respectively. We have previously shown that RPS3 and RPM1 are closely linked genetically. Here, we show that RPS3 and RPM1 are in fact the same gene. We screened a mutagenized Arabidopsis population with a P. syringae strain carrying avrB and found 12 susceptible mutants. All 12 mutants were also susceptible to an isogenic strain carrying avrRpm1, indicating a loss of both RPS3 and RPM1 functions. No mutants were recovered that lost only RPS3 function. Genetic analysis of four independent mutants revealed that the lesions were in RPS3. Thus, a single gene in Arabidopsis confers resistance that is specific to two distinct pathogen avirulence genes--a gene-for-genes interaction. This observation suggests that the RPS3/RPM1 gene product can bind multiple pathogen ligands, or alternatively, that it does not function as a receptor.     

The Tarenaya hassleriana Genome Provides Insight into Reproductive Trait and Genome Evolution of Crucifers

The Brassicaceae, including Arabidopsis thaliana and Brassica crops, is unmatched among plants in its wealth of genomic and functional molecular data and has long served as a model for understanding gene, genome, and trait evolution. However, genome information from a phylogenetic outgroup that is essential for inferring directionality of evolutionary change has been lacking. We therefore sequenced the genome of the spider flower (Tarenaya hassleriana) from the Brassicaceae sister family, the Cleomaceae. By comparative analysis of the two lineages, we show that genome evolution following ancient polyploidy and gene duplication events affect reproductively important traits. We found an ancient genome triplication in Tarenaya (Th-α) that is independent of the Brassicaceae-specific duplication (At-α) and nested Brassica (Br-α) triplication. To showcase the potential of sister lineage genome analysis, we investigated the state of floral developmental genes and show Brassica retains twice as many floral MADS (for MINICHROMOSOME MAINTENANCE1, AGAMOUS, DEFICIENS and SERUM RESPONSE FACTOR) genes as Tarenaya that likely contribute to morphological diversity in Brassica. We also performed synteny analysis of gene families that confer self-incompatibility in Brassicaceae and found that the critical SERINE RECEPTOR KINASE receptor gene is derived from a lineage-specific tandem duplication. The T. hassleriana genome will facilitate future research toward elucidating the evolutionary history of Brassicaceae genomes.     

Isolation of NBS-LRR RGAs from invasive Wedelia trilobata and the calculation of evolutionary rates to understand bioinvasion from a molecular evolution perspective

Supports for the molecular evolution of host–pathogen interactions on enemy release hypothesis are rare. According to the theory of plant immunity and the coevolution of hosts and pathogens, we hypothesized that the evolutionary rate (d_N/d_S) of resistance genes (R-genes) in invasive plants would be greater than in non-invasive plants, assuming that based on the enemy release hypothesis, the former would suffer less selection stress from co-evolutionary specialist pathogens. To test our hypothesis, we isolated and analyzed the conserved nucleotide-binding sites (NBS) of resistance gene analogues (RGAs) of an invasive weed, Wedelia trilobata (WTRGA). We then used the information in GenBank to compare the d_N/d_S of the NBS R-gene/RGAs in invasive and homologous non-invasive plants. Three W. trilobata NBS RGA sequences were obtained, belonging to the Toll/Interleukin-1 receptor (TIR) (WTRGA1 and WTRGA2) and non-TIR subclasses (WTRGA3). Compared with the homologous non-invasive plants, the invasive plants showed a significantly greater d_N/d_S for TIR NBS R-gene/RGAs (p < 0.0001), supporting our hypothesis. Future research should include an examination of R-genes/RGAs from more invasive plants on a population level to understand diversity and R-gene functions in invasive plant species, as well as to explore how disease resistance allows plants to adapt to changing pathogen stresses.     

Mechanism of resistance induced by plant activators against Colletotrichum falcatum in sugarcane

Abstract

A search for plant activators capable of inducing systemic resistance in sugarcane showed that plants pre-treated with synthetic signal inducers confer a high degree of resistance to Colletotrichum falcatum – the red rot pathogen. Among the various treatments, Acibenzolar S- methyl (ASM) was found to be very effective in restricting the pathogen colonization inside the inoculated cane stalk tissues. The induction of resistance was accompanied by a significant increase in peroxidases and polyphenoloxidases activities. A considerable decrease of pathogen titre in the pre-treated tissues as determined by ELISA, clearly demonstrated the restriction of pathogen colonization and proliferation in the sensitized cane stalks. Specific induction of new isoforms of peroxidases and polyphenoloxidases in C. falcatum elicitor treatment indicates the pathogen elicitor induced specific cellular response of sugarcane suspension-cultured cells.