Transmission rates and adaptive evolution of pathogens in sympatric heterogeneous plant populations.
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Diversification in agricultural cropping patterns is widely practised to delay the build-up of virulent races that can overcome host resistance in pathogen populations. This can lead to balanced polymorphism, but the long-term consequences of this strategy for the evolution of crop pathogen populations are still unclear. The widespread occurrence of sibling species and reproductively isolated sub-species among fungal and oomycete plant pathogens suggests that evolutionary divergence is common. This paper develops a mathematical model of host-pathogen interactions using a simple framework of two hosts to analyse the influences of sympatric host heterogeneity on the long-term evolutionary behaviour of plant pathogens. Using adaptive dynamics, which assumes that sequential mutations induce small changes in pathogen fitness, we show that evolutionary outcomes strongly depend on the shape of the trade-off curve between pathogen transmission on sympatric hosts. In particular, we determine the conditions under which the evolutionary branching of a monomorphic into a dimorphic population occurs, as well as the conditions that lead to the evolution of specialist (single host range) or generalist (multiple host range) pathogen populations. (+info)
Induction of a sunflower CC-NBS-LRR resistance gene analogue during incompatible interaction with Plasmopara halstedii.
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Downy mildew caused by Plasmopara halstedii is one of the main diseases causing economic losses in cultivated sunflower. Resistance in this host is conferred by major genes denoted Pl. The inbred sunflower line QIR8, which contains the Pl8 locus and is resistant to all known downy mildew races, was used to isolate a full-length resistance gene analogue (RGA) belonging to the CC-NBC-LRR class of plant resistance genes. The genetically incompatible combination involving downy mildew races 300 and sunflower line QIR8 was characterized by a hypersensitive-like reaction. Semi-quantitative RT-PCR analysis showed that the transcript of Ha-NTIR11g RGA was specifically induced during the incompatible reaction. The transcript was induced approximately 3 d post-infection (dpi), and then decreased by 9 dpi. The high level of transcriptional expression of this RGA coincides with a transcript accumulation of the hsr203J gene which is a marker of the hypersensitive reaction. Treatment with signalling molecules, including salicylic acid and methyl jasmonate, did not activate transcription of the Ha-NTIR11g gene, indicating that Ha-NTIR11g expression is not regulated by defence signalling pathways triggered by these molecules. Ha-NTIR11g was not induced by treatment with hydrogen peroxide or wounding. These results suggest that Ha-NTIR11g RGA may play a critical role in protecting sunflower cells against P. halstedii. The transcript accumulation of R gene-mediated signalling components was also examined. (+info)
Host-parasite coevolutionary conflict between Arabidopsis and downy mildew.
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Plants are constantly exposed to attack by an array of diverse pathogens but lack a somatically adaptive immune system. In spite of this, natural plant populations do not often suffer destructive disease epidemics. Elucidating how allelic diversity within plant genes that function to detect pathogens (resistance genes) counteracts changing structures of pathogen genes required for host invasion (pathogenicity effectors) is critical to our understanding of the dynamics of natural plant populations. The RPP13 resistance gene is the most polymorphic gene analyzed to date in the model plant Arabidopsis thaliana. Here we report the cloning of the avirulence gene, ATR13, that triggers RPP13-mediated resistance, and we show that it too exhibits extreme levels of amino acid polymorphism. Evidence of diversifying selection visible in both components suggests that the host and pathogen may be locked in a coevolutionary conflict at these loci, where attempts to evade host resistance by the pathogen are matched by the development of new detection capabilities by the host. (+info)
Dissecting the beta-aminobutyric acid-induced priming phenomenon in Arabidopsis.
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Plants treated with the nonprotein amino acid beta-aminobutyric acid (BABA) develop an enhanced capacity to resist biotic and abiotic stresses. This BABA-induced resistance (BABA-IR) is associated with an augmented capacity to express basal defense responses, a phenomenon known as priming. Based on the observation that high amounts of BABA induce sterility in Arabidopsis thaliana, a mutagenesis screen was performed to select mutants impaired in BABA-induced sterility (ibs). Here, we report the isolation and subsequent characterization of three T-DNA-tagged ibs mutants. Mutant ibs1 is affected in a cyclin-dependent kinase-like protein, and ibs2 is defective in AtSAC1b encoding a polyphosphoinositide phosphatase. Mutant ibs3 is affected in the regulation of the ABA1 gene encoding the abscisic acid (ABA) biosynthetic enzyme zeaxanthin epoxidase. To elucidate the function of the three IBS genes in plant resistance, the mutants were tested for BABA-IR against the bacterium Pseudomonas syringae pv tomato, the oomycete Hyaloperonospora parasitica, and BABA-induced tolerance to salt. All three ibs mutants were compromised in BABA-IR against H. parasitica, although to a different extent. Whereas ibs1 was reduced in priming for salicylate (SA)-dependent trailing necrosis, mutants ibs2 and ibs3 were affected in the priming for callose deposition. Only ibs1 failed to express BABA-IR against P. syringae, which coincided with a defect in priming for SA-inducible PR-1 gene expression. By contrast, ibs2 and ibs3 showed reduced BABA-induced tolerance to salt, which correlated with an affected priming for ABA-inducible gene expression. For all three ibs alleles, the defects in BABA-induced sterility and BABA-induced protection against P. syringae, H. parasitica, and salt could be confirmed in independent mutants. The data presented here introduce three novel regulatory genes involved in priming for different defense responses. (+info)
Diagnostic application of padlock probes--multiplex detection of plant pathogens using universal microarrays.
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Padlock probes (PLPs) are long oligonucleotides, whose ends are complementary to adjacent target sequences. Upon hybridization to the target, the two ends are brought into contact, allowing PLP circularization by ligation. PLPs provide extremely specific target recognition, which is followed by universal amplification and microarray detection. Since target recognition is separated from downstream processing, PLPs enable the development of flexible and extendable diagnostic systems, targeting diverse organisms. To adapt padlock technology for diagnostic purposes, we optimized PLP design to ensure high specificity and eliminating ligation on non-target sequences under real-world assay conditions. We designed and tested 11 PLPs to target various plant pathogens at the genus, species and subspecies levels, and developed a prototype PLP-based plant health chip. Excellent specificity was demonstrated toward the target organisms. Assay background was determined for each hybridization using a no-target reference sample, which provided reliable and sensitive identification of positive samples. A sensitivity of 5 pg genomic DNA and a dynamic range of detection of 100 were observed. The developed multiplex diagnostic system was validated using genomic DNAs of characterized isolates and artificial mixtures thereof. The demonstrated system is adaptable to a wide variety of applications ranging from pest management to environmental microbiology. (+info)
An importin alpha homolog, MOS6, plays an important role in plant innate immunity.
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Plant disease resistance is the consequence of an innate defense mechanism mediated by Resistance (R) genes [1]. The conserved structure of one class of R protein is reminiscent of Toll-like receptors (TLRs) and Nucleotide binding oligomerization domain (NOD) proteins-immune-response perception modules in animal cells [2, 3, and 4]. The Arabidopsis snc1 (suppressor of npr1-1, constitutive, 1) mutant contains a mutation in a TIR-NBS-LRR-type of R gene that renders resistance responses constitutively active without interaction with pathogens [5]. Few components of the downstream signaling network activated by snc1 are known. To search for regulators of R-gene-mediated resistance, we screened for genetic suppressors of snc1. Three alleles of the mutant mos6 (modifier of snc1, 6) partially suppressed constitutive-resistance responses and immunity to virulent pathogens in snc1. Furthermore, the mos6-1 single mutant exhibited enhanced disease susceptibility to a virulent oomycete pathogen. MOS6, identified by positional cloning, encodes importin alpha3, one of eight alpha importins in Arabidopsis [6]. alpha importins mediate the import of specific proteins across the nuclear envelope. We previously reported that MOS3, a protein homologous to human nucleoporin 96, is required for constitutive resistance in snc1 [7]. Our data highlight an essential role for nucleo-cytoplasmic trafficking, especially protein import, in plant innate immunity. (+info)
Identification of arabidopsis loci required for susceptibility to the downy mildew pathogen Hyaloperonospora parasitica.
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Plants are susceptible to a limited number of pathogens. Most infections fail due to active defense or absence of compatibility. Many components of the plant's surveillance system and defense arsenal have been identified in the last decades. However, knowledge is limited on compatibility; in particular, the role of plant factors in the infection process. To gain insight into these processes, we have initiated an Arabidopsis thaliana mutant screen for reduced susceptibility to the downy mildew pathogen Hyaloperonospora parasitica. Ethyl methane sulfonate (EMS) mutants were generated in the highly susceptible Arabidopsis line Ler eds1-2. Eight downy mildew-resistant (dmr) mutants were analyzed in detail, corresponding to six different loci. Microscopic analysis showed that, in all mutants, H. parasitica growth was severely reduced. Resistance of dmr3, dmr4, and dmr5 was associated with constitutive expression of PR-1. Furthermore, dmr3 and dmr4, but not dmr5, also were resistant to Pseudomonas syringae and Golovinomyces orontii, respectively. However, enhanced activation of plant defense was not observed in dmr1, dmr2, and dmr6. We postulate that, in these susceptibility mutants, cellular processes are disrupted which are required for H. parasitica infection. This interesting new set of mutants provides a basis to elucidate the molecular processes underlying susceptibility to downy mildew in Arabidopsis. (+info)
Suppression of damping-off disease in host plants by the rhizoplane bacterium Lysobacter sp. strain SB-K88 is linked to plant colonization and antibiosis against soilborne Peronosporomycetes.
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We previously demonstrated that xanthobaccin A from the rhizoplane bacterium Lysobacter sp. strain SB-K88 suppresses damping-off disease caused by Pythium sp. in sugar beet. In this study we focused on modes of Lysobacter sp. strain SB-K88 root colonization and antibiosis of the bacterium against Aphanomyces cochlioides, a pathogen of damping-off disease. Scanning electron microscopic analysis of 2-week-old sugar beet seedlings from seeds previously inoculated with SB-K88 revealed dense colonization on the root surfaces and a characteristic perpendicular pattern of Lysobacter colonization possibly generated via development of polar, brush-like fimbriae. In colonized regions a semitransparent film apparently enveloping the root and microcolonies were observed on the root surface. This Lysobacter strain also efficiently colonized the roots of several plants, including spinach, tomato, Arabidopsis thaliana, and Amaranthus gangeticus. Plants grown from both sugar beet and spinach seeds that were previously treated with Lysobacter sp. strain SB-K88 displayed significant resistance to the damping-off disease triggered by A. cochlioides. Interestingly, zoospores of A. cochlioides became immotile within 1 min after exposure to a SB-K88 cell suspension, a cell-free supernatant of SB-K88, or pure xanthobaccin A (MIC, 0.01 microg/ml). In all cases, lysis followed within 30 min in the presence of the inhibiting factor(s). Our data indicate that Lysobacter sp. strain SB-K88 has a direct inhibitory effect on A. cochlioides, suppressing damping-off disease. Furthermore, this inhibitory effect of Lysobacter sp. strain SB-K88 is likely due to a combination of antibiosis and characteristic biofilm formation at the rhizoplane of the host plant. (+info)