Infection of plants by necrotizing pathogens or colonization of plant roots with certain beneficial microbes causes the induction of a unique physiological state called "priming." The primed state can also be induced by treatment of plants with various natural and synthetic compounds. Primed plants display either faster, stronger, or both activation of the various cellular defense responses that are induced following attack by either pathogens or insects or in response to abiotic stress. Although the phenomenon has been known for decades, most progress in our understanding of priming has been made over the past few years. Here, we summarize the current knowledge of priming in various induced-resistance phenomena in plants.
Lack of the barley (Hordeum vulgare) seven-transmembrane domain MLO protein confers resistance against the fungal pathogen Blumeria graminis f. sp. hordei (Bgh). To broaden the basis for MLO structure/function studies, we sequenced additional mlo resistance alleles, two of which confer only partial resistance. Wild-type MLO dampens the cell wall-restricted hydrogen peroxide burst at points of attempted fungal penetration of the epidermal cell wall, and in subtending mesophyll cells, it suppresses a second oxidative burst and cell death. Although the Bgh-induced cell death in mlo plants is spatially and temporally separated from resistance, we show that the two processes are linked. Uninoculated mutant mlo plants exhibit spontaneous mesophyll cell death that appears to be part of accelerated leaf senescence. Mlo transcript abundance increases in response to Bgh, rice (Oryza sativa) blast, wounding, paraquat treatment, a wheat powdery mildew-derived carbohydrate elicitor, and during leaf senescence. This suggests a broad involvement of Mlo in cell death protection and in responses to biotic and abiotic stresses.Homozygous mutant (mlo) alleles of the Mlo gene confer broad spectrum disease resistance to the biotrophic powdery mildew fungus, Blumeria graminis f. sp. hordei (Bgh; Jørgensen, 1992). The resistance is manifested in the failure of the fungus to penetrate the epidermal cell wall, and at these sites, cell wall remodeling and oxidative cross-linking processes fortify the cell wall (Thordal-Christensen et al., 1997; von Rö penack et al., 1998; Hü ckelhoven et al., 1999). Although cell wall reinforcement is likely to contribute to the resistant phenotype, other yet unknown molecular events may lead to abortion of fungal attack. Although the wild-type Mlo gene in effect acts as a negative regulator of a defense response, wildtype Ror1 and Ror2 are two genes that are required for full expression of mlo resistance to Bgh, but not race-specific resistance (Freialdenhoven et al., 1996; Peterhänsel et al., 1997). It is curious that powdery mildew-resistant mlo plants exhibit enhanced susceptibility to the fungal pathogens Magnaporthe grisea and Bipolaris sorokiniana (Jarosch et al., 1999; Kumar et al., 2001).Mutant mlo plants exhibit a spontaneous mesophyll cell death phenotype that is compromised by ror1 and ror2 mutations (Wolter et al., 1993; Peterhänsel et al., 1997). In this respect, mlo mutations resemble other mutations known to enhance host cell death processes along with disease resistance (Shirasu and SchulzeLefert, 2000). Many of these mutants constitutively express pathogen-related (PR) genes, but in barley (Hordeum vulgare) mlo, maize (Zea mays) lls1, and Arabidopsis lsd1 and edr1 plants, pathogen inoculation is required to trigger an enhanced defense response (Jabs et al., 1996; Frye and Innes, 1998; Simmons et al., 1998). These four genes have been isolated (Bü schges et al., 1997; Dietrich et al., 1997; Gray et al., 1997; Frye et al., 2001), and encode dissimilar proteins.Barley MLO is the pro...
At the beginning of the disease, small, tan-coloured lesions, restricted by leaf veins, can be observed on infected soybean leaves. Lesions enlarge and, 5-8 days after initial infection, rust pustules (uredia, syn. uredinia) become visible. Uredia develop more frequently in lesions on the lower surface of the leaf than on the upper surface. The uredia open with a round ostiole through which uredospores are released.
Recessive alleles of the barley Mlo locus confer non-race-specific resistance against the powdery mildew fungus Blumeria graminis f. sp. hordei (Bgh). Recently the Mlo gene has been isolated and it was suggested that the Mlo product is a negative regulator of cell death. Thus, loss of function can precondition cells to a higher responsiveness for the onset of multiple defense functions. Here, we document an enhanced susceptibility of barley mlo mutants to the rice blast fungus Magnaporthe grisea. The disease phenotype is independent of the barley cultivar in which the mlo allele has been introgressed and occurs in equal amounts in barley backcross lines of cv. Ingrid carrying the mlo-1, mlo-3, or mlo-5 allele. Ror genes, which are required for the full expression of mlo resistance in barley against Bgh, do not affect the specific mlo-mediated phenotype observed after M. grisea infection. Formation of an effective papilla restricts blast development in epidermal cells of Mlo plants. In contrast, papillae are mostly penetrated in mlo mutants and, as a consequence, the fungus spreads into adjacent mesophyll cells. Both wild-type plants and mlo mutants did not differ in perception of a purified elicitor derived from M. grisea. Thus, we hypothesize that a functional Mlo protein is a prerequisite for penetration resistance of barley to fungal pathogens like M. grisea. The benefit of mlo alleles for durable resistance in barley and a proposed role of mlo-type-mutations in rice are discussed.
Asian soybean rust (ASR), caused by Phakopsora pachyrhizi, is a devastating disease of soybean. We report the use of the nonhost plant Arabidopsis thaliana to identify the genetic basis of resistance to P. pachyrhizi. Upon attack by P. pachyrhizi, epidermal cells of wild-type Arabidopsis accumulated H2O2, which likely orchestrates the frequently observed epidermal cell death. However, even when epidermal cell death occurred, fungal hyphae grew on and infection was terminated at the mesophyll boundary. These events were associated with expression of PDF1.2, suggesting that P. pachyrhizi, an ostensible biotroph, mimics aspects of a necrotroph. Extensive colonization of the mesophyll occurred in Arabidopsis pen mutants with defective penetration resistance. Although haustoria were found occasionally in mesophyll cells, the successful establishment of biotrophy failed, as evidenced by the cessation of fungal growth. Double mutants affected in either jasmonic acid or salicylic acid signaling in the pen3-1 background revealed the involvement of both pathways in nonhost resistance (NHR) of Arabidopsis to P. pachyrhizi. Interestingly, expression of AtNHL10, a gene that is expressed in tissue undergoing the hypersensitive response, was only triggered in infected pen3-1 mutants. Thus, a suppression of P. pachyrhizi-derived effectors by PEN3 can be inferred. Our results demonstrate that Arabidopsis can be used to study mechanisms of NHR to ASR.
Summary The wheat gene Lr34 confers durable and partial field resistance against the obligate biotrophic, pathogenic rust fungi and powdery mildew in adult wheat plants. The resistant Lr34 allele evolved after wheat domestication through two gain‐of‐function mutations in an ATP‐binding cassette transporter gene. An Lr34‐like fungal disease resistance with a similar broad‐spectrum specificity and durability has not been described in other cereals. Here, we transformed the resistant Lr34 allele into the japonica rice cultivar Nipponbare. Transgenic rice plants expressing Lr34 showed increased resistance against multiple isolates of the hemibiotrophic pathogen Magnaporthe oryzae, the causal agent of rice blast disease. Host cell invasion during the biotrophic growth phase of rice blast was delayed in Lr34‐expressing rice plants, resulting in smaller necrotic lesions on leaves. Lines with Lr34 also developed a typical, senescence‐based leaf tip necrosis (LTN) phenotype. Development of LTN during early seedling growth had a negative impact on formation of axillary shoots and spikelets in some transgenic lines. One transgenic line developed LTN only at adult plant stage which was correlated with lower Lr34 expression levels at seedling stage. This line showed normal tiller formation and more importantly, disease resistance in this particular line was not compromised. Interestingly, Lr34 in rice is effective against a hemibiotrophic pathogen with a lifestyle and infection strategy that is different from obligate biotrophic rusts and mildew fungi. Lr34 might therefore be used as a source in rice breeding to improve broad‐spectrum disease resistance against the most devastating fungal disease of rice.
Nonhost resistance protects plants against attack by the vast majority of potential pathogens, including phytopathogenic fungi. Despite its high biological importance, the molecular architecture of nonhost resistance has remained largely unexplored. Here, we describe the transcriptional responses of one particular genotype of barley (Hordeum vulgare subsp. vulgare 'Ingrid') to three different pairs of adapted (host) and nonadapted (nonhost) isolates of fungal pathogens, which belong to the genera Blumeria (powdery mildew), Puccinia (rust), and Magnaporthe (blast). Nonhost resistance against each of these pathogens was associated with changes in transcript abundance of distinct sets of nonhost-specific genes, although general (not nonhost-associated) transcriptional responses to the different pathogens overlapped considerably. The powdery mildew- and blast-induced differences in transcript abundance between host and nonhost interactions were significantly correlated with differences between a near-isogenic pair of barley lines that carry either the Mlo wild-type allele or the mutated mlo5 allele, which mediates basal resistance to powdery mildew. Moreover, during the interactions of barley with the different host or nonhost pathogens, similar patterns of overrepresented and underrepresented functional categories of genes were found. The results suggest that nonhost resistance and basal host defense of barley are functionally related and that nonhost resistance to different fungal pathogens is associated with more robust regulation of complex but largely nonoverlapping sets of pathogen-responsive genes involved in similar metabolic or signaling pathways.
CRISPR/Cas has become the state-of-the-art technology for genetic manipulation in diverse organisms, enabling targeted genetic changes to be performed with unprecedented efficiency. Here we report on the first establishment of robust CRISPR/Cas editing in the important necrotrophic plant pathogen Botrytis cinerea based on the introduction of optimized Cas9-sgRNA ribonucleoprotein complexes (RNPs) into protoplasts. Editing yields were further improved by development of a novel strategy that combines RNP delivery with cotransformation of transiently stable vectors containing telomeres, which allowed temporary selection and convenient screening for marker-free editing events. We demonstrate that this approach provides superior editing rates compared to existing CRISPR/Cas-based methods in filamentous fungi, including the model plant pathogen Magnaporthe oryzae. Genome sequencing of edited strains revealed very few additional mutations and no evidence for RNP-mediated off-targeting. The high performance of telomere vector-mediated editing was demonstrated by random mutagenesis of codon 272 of the sdhB gene, a major determinant of resistance to succinate dehydrogenase inhibitor (SDHI) fungicides by in bulk replacement of the codon 272 with codons encoding all 20 amino acids. All exchanges were found at similar frequencies in the absence of selection but SDHI selection allowed the identification of novel amino acid substitutions which conferred differential resistance levels towards different SDHI fungicides. The increased efficiency and easy handling of RNPbased cotransformation is expected to accelerate molecular research in B. cinerea and other fungi.
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