Comparative pathobiology approaches to generating transgenic crop plants with enhanced resistance to fungal pathogens

2003 ◽  
Vol 31 (4) ◽  
pp. 319-323 ◽  
Author(s):  
Martin Dickman
2004 ◽  
Vol 17 (11) ◽  
pp. 1242-1249 ◽  
Author(s):  
Phil H. Smith ◽  
John A. Howie ◽  
Anthony J. Worland ◽  
Rebecca Stratford ◽  
Lesley A. Boyd

Two mutants were isolated in wheat that showed enhanced resistance towards Puccinia striiformis f. sp. tritici, the fungal causal agent of yellow rust. The altered phenotype of I3-48 is due to a minimum of two mutation events, each showing a partial, additive effect, with one mutation segregating with a deletion on the long arm of chromosome 4D. In the case of I3-54, the enhanced resistance is due to a single, dominant mutation. In both mutants, the expression of the enhanced resistance is growth-stage specific. With I3-54, the full resistance phenotype is apparent from the third seedling leaf onwards, while with I3-48, a full resistance phenotype is only seen on the tenth and subsequent leaves. In addition to the enhanced resistance towards yellow rust, I3-48 also shows enhanced resistance towards brown rust, and I3-54 shows enhanced resistance to powdery mildew.


2018 ◽  
Vol 23 (9) ◽  
pp. 753-755 ◽  
Author(s):  
Isabelle Fudal ◽  
Marie-Hélène Balesdent ◽  
Thierry Rouxel
Keyword(s):  

2007 ◽  
Vol 20 (8) ◽  
pp. 966-976 ◽  
Author(s):  
Wenming Wang ◽  
Alessandra Devoto ◽  
John G. Turner ◽  
Shunyuan Xiao

The powdery mildew resistance genes RPW8.1 and RPW8.2 from Arabidopsis differ from the other isolated plant resistance (R) genes in their predicted protein domains and their resistance spectrum. The two homologous RPW8 genes encode small proteins featuring a predicted amino-terminal transmembrane anchor domain and a coiled-coil domain and confer resistance to a broad spectrum of powdery mildews. Here, we show that Arabidopsis plants expressing the RPW8 genes have enhanced resistance to another biotrophic pathogen, Hyaloperonospora parasitica, raising the possibility that the RPW8 genes may function to enhance salicylic-acid-dependent basal defenses, rather than as powdery-mildew-specific R genes. When overexpressed from their native promoters, the RPW8 genes confer enhanced resistance to the Cauliflower mosaic virus, but render plants more susceptible to the necrotrophic fungal pathogens Alternaria and Botrytis spp. Furthermore, we show that the RPW8 proteins appear to be localized to the endomembrane system, overlapping with the endoplasmic reticulum–associated small GTPase SAR1, and accumulate to higher levels in response to application of exogenous salicylic acid, one of the signaling molecules of plant defense.


2011 ◽  
Vol 29 (6) ◽  
pp. 703-714 ◽  
Author(s):  
P. Manimaran ◽  
G. Ramkumar ◽  
K. Sakthivel ◽  
R.M. Sundaram ◽  
M.S. Madhav ◽  
...  

2015 ◽  
Vol 14 (3) ◽  
pp. 875-886 ◽  
Author(s):  
Emily E. Helliwell ◽  
Julio Vega-Arreguín ◽  
Zi Shi ◽  
Bryan Bailey ◽  
Shunyuan Xiao ◽  
...  

1999 ◽  
Vol 12 (12) ◽  
pp. 1053-1063 ◽  
Author(s):  
Herman Silva ◽  
Keiko Yoshioka ◽  
Hugo K. Dooner ◽  
Daniel F. Klessig

In many plant-pathogen interactions, resistance is associated with the synthesis and accumulation of salicylic acid (SA) and pathogenesis-related (PR) proteins. At least two general classes of mutants with altered resistance to pathogen attack have been identified in Arabidopsis. One class exhibits increased susceptibility to pathogen infection; the other class exhibits enhanced resistance to pathogens. In an attempt to identify mutations in resistance-associated loci, we screened a population of T-DNA tagged Arabidopsis thaliana ecotype Wassilewskija (Ws) for mutants showing constitutive expression of the PR-1 gene (cep). A mutant was isolated and shown to constitutively express PR-1, PR-2, and PR-5 genes. This constitutive phenotype segregated as a single recessive trait in the Ws genetic background. The mutant also had elevated levels of SA, which are responsible for the cep phenotype. The cep mutant spontaneously formed hypersensitive response (HR)-like lesions on the leaves and cotyledons and also exhibited enhanced resistance to virulent bacterial and fungal pathogens. Genetic analyses of segregating progeny from outcrosses to other ecotypes unexpectedly revealed that alterations in more than one gene condition the constitutive expression of PR genes in the original mutant. One of the mutations, designated cpr20, maps to the lower arm of chromosome 4 and is required for the cep phenotype. Another mutation, which has been termed cpr21, maps to chromosome 1 and is often, but not always, associated with this phenotype. The recessive nature of the cep trait suggests that the CPR20 and CPR21 proteins may act as negative regulators in the disease resistance signal transduction pathway.


2000 ◽  
Vol 55 (7-8) ◽  
pp. 552-559 ◽  
Author(s):  
Udo Roth ◽  
Annette Friebe ◽  
Heide Schnabl

Abstract Resistance inducing effects of an extract of Lychnis viscaria L. seeds, containing different brassinosteroids (BR), were investigated. Application of aqueous solutions in concentrations from 0.5 to 10 mg/l (dry wt. of extract) resulted in an enhanced resistance of tobacco, cucumber and tomato to viral and fungal pathogens of up to 36% compared with water-treated control plants. No direct anti-fungal effects in mycelium growth assays with Phytophthora infestans could be observed. After treatment and inoculation with powdery mildew a stimulation of different PR-proteins (ca. + 20% for peroxidase, + 30% for chitinase and up to + 68% for β-1,3-glucanase) in cucumber was found. A chitinase in gel-electrophoresisassay showed a stronger induction of a distinct isoform under the same conditions. Time course of peroxidase induction and changes of apoplastic protein patterns revealed by SDS-PAGE indicated an earlier triggering of defence responses after plant-extract treatment and pathogen attack, probably being responsible for the increased resistance. Involvement of the brassinosteroids in the plant extract is discussed to elicit or mediate the activation of defence-mechanisms.


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