A Conserved Hypothetical Gene Is Required but Not Sufficient for Ptr ToxC Production in .

The fungus causes tan spot, an important foliar disease of wheat worldwide. The fungal pathogen produces three necrotrophic effectors, namely Ptr ToxA, Ptr ToxB, and Ptr ToxC to induce necrosis or chlorosis in wheat. Both Ptr ToxA and Ptr ToxB are proteins, and their encoding genes have been cloned.

A genome-wide genetic linkage map and reference quality genome sequence for a new race in the wheat pathogen Pyrenophora tritici-repentis.

Pyrenophora tritici-repentis is an ascomycete fungus that causes tan spot of wheat. The disease has a worldwide distribution and can cause significant yield and quality losses in wheat production. The fungal pathogen is homothallic in nature, which means it can undergo sexual reproduction by selfing to produce pseudothecia on wheat stubble for seasonal survival.

Molecular and Cytogenetic Characterization of Six Wheat- Disomic Addition Lines and Their Resistance to Rusts and Powdery Mildew.

(Greuter) Hammer is an important source of genes for resistance to abiotic stresses and diseases in wheat ( L.). A series of six wheat 'Alcedo'- chromosome disomic addition lines, designated as AI(B), AII(C), AIII(D), AV(E), AIV(F), and AVIII(G) carrying the .

Molecular manipulation of the mating-type system and development of a new approach for characterizing pathogen virulence in Pyrenophora tritici-repentis.

The ascomycete Pyrenophora tritici-repentis (Ptr) is an important fungal pathogen worldwide that causes tan spot of wheat. The fungus is self-fertile because each isolate contains both mating type (MAT) idiomorphs. In this work, we developed knockouts of the MAT genes in Ptr and tested fertility of the knockout strains and outcrossing between the knockout strains carrying the opposite mating type.

Inverse gene-for-gene interactions contribute additively to tan spot susceptibility in wheat.

Tan spot susceptibility is conferred by multiple interactions of necrotrophic effector and host sensitivity genes. Tan spot of wheat, caused by Pyrenophora tritici-repentis, is an important disease in almost all wheat-growing areas of the world. The disease system is known to involve at least three fungal-produced necrotrophic effectors (NEs) that interact with the corresponding host sensitivity (S) genes in an inverse gene-for-gene manner to induce disease.

The hijacking of a receptor kinase-driven pathway by a wheat fungal pathogen leads to disease.

Necrotrophic pathogens live and feed on dying tissue, but their interactions with plants are not well understood compared to biotrophic pathogens. The wheat gene confers susceptibility to strains of the necrotrophic pathogen that produce the SnTox1 protein. We report the positional cloning of , a member of the wall-associated kinase class of receptors, which are known to drive pathways for biotrophic pathogen resistance.

Genetic relationships between race-nonspecific and race-specific interactions in the wheat-Pyrenophora tritici-repentis pathosystem.

We identified a major QTL conferring race-nonspecific resistance and revealed its relationships with race-specific interactions in the wheat- Pyrenophora tritici-repentis pathosystem. Tan spot, caused by the fungus Pyrenophora tritici-repentis (Ptr), is a destructive disease of wheat worldwide. The disease system is known to include inverse gene-for-gene, race-specific interactions involving the recognition of fungal-produced necrotrophic effectors (NEs) by corresponding host sensitivity genes.

Development of a diagnostic co-dominant marker for stem rust resistance gene Sr47 introgressed from Aegilops speltoides into durum wheat.

A robust and diagnostic STS marker for stem rust resistance gene Sr47 was developed and validated for marker-assisted selection. Stem rust (caused by Puccinia graminis f. sp.

Marker development, saturation mapping, and high-resolution mapping of the Septoria nodorum blotch susceptibility gene Snn3-B1 in wheat.

Septoria nodorum blotch (SNB), caused by Parastagonospora nodorum, is a severe foliar and glume disease on durum and common wheat. Pathogen-produced necrotrophic effectors (NEs) are the major determinants for SNB on leaves. One such NE is SnTox3, which evokes programmed cell death and leads to disease when recognized by the wheat Snn3-B1 gene.

Identification and mapping of Sr46 from Aegilops tauschii accession CIae 25 conferring resistance to race TTKSK (Ug99) of wheat stem rust pathogen.

Mapping studies confirm that resistance to Ug99 race of stem rust pathogen in Aegilops tauschii accession Clae 25 is conditioned by Sr46 and markers linked to the gene were developed for marker-assisted selection. The race TTKSK (Ug99) of Puccinia graminis f. sp.

Duplication and partitioning in evolution and function of homoeologous Q loci governing domestication characters in polyploid wheat.

The Q gene encodes an AP2-like transcription factor that played an important role in domestication of polyploid wheat. The chromosome 5A Q alleles (5AQ and 5Aq) have been well studied, but much less is known about the q alleles on wheat homoeologous chromosomes 5B (5Bq) and 5D (5Dq). We investigated the organization, evolution, and function of the Q/q homoeoalleles in hexaploid wheat (Triticum aestivum L.

Variable expression of the Stagonospora nodorum effector SnToxA among isolates is correlated with levels of disease in wheat.

Most research on host?pathogen interactions is focused on mechanisms of resistance, but less is known regarding mechanisms of susceptibility. The wheat?Stagonospora nodorum pathosystem involves pathogen-produced effectors, also known as host-selective toxins, that interact with corresponding dominant host genes to cause disease. Recognition of the S.

RNA-mediated gene silencing in the cereal fungal pathogen Cochliobolus sativus.

A high-throughput RNA-mediated gene silencing system was developed for Cochliobolus sativus (anamorph: Bipolaris sorokiniana), the causal agent of spot blotch, common root rot and black point in barley and wheat. The green fluorescent protein gene (GFP) and the proteinaceous host-selective toxin gene (ToxA) were first introduced into C. sativus via the polyethylene glycol (PEG)-mediated transformation method.

Two putatively homoeologous wheat genes mediate recognition of SnTox3 to confer effector-triggered susceptibility to Stagonospora nodorum.

The pathogen Stagonospora nodorum produces multiple effectors, also known as host-selective toxins (HSTs), that interact with corresponding host sensitivity genes in an inverse gene-for-gene manner to cause the disease Stagonospora nodorum blotch (SNB) in wheat. In this study, a sensitivity gene was identified in Aegilops tauschii, the diploid D-genome donor of common wheat. The gene was mapped to the short arm of chromosome 5D and mediated recognition of the effector SnTox3, which was previously shown to be recognized by the wheat gene Snn3 on chromosome arm 5BS.

A unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens.

Plant disease resistance is often conferred by genes with nucleotide binding site (NBS) and leucine-rich repeat (LRR) or serine/threonine protein kinase (S/TPK) domains. Much less is known about mechanisms of susceptibility, particularly to necrotrophic fungal pathogens. The pathogens that cause the diseases tan spot and Stagonospora nodorum blotch on wheat produce effectors (host-selective toxins) that induce susceptibility in wheat lines harboring corresponding toxin sensitivity genes.

SnTox3 acts in effector triggered susceptibility to induce disease on wheat carrying the Snn3 gene.

The necrotrophic fungus Stagonospora nodorum produces multiple proteinaceous host-selective toxins (HSTs) which act in effector triggered susceptibility. Here, we report the molecular cloning and functional characterization of the SnTox3-encoding gene, designated SnTox3, as well as the initial characterization of the SnTox3 protein. SnTox3 is a 693 bp intron-free gene with little obvious homology to other known genes.

Tsn1-mediated host responses to ToxA from Pyrenophora tritici-repentis.

The toxin sensitivity gene Tsn1 interacts with Ptr ToxA (ToxA), a host-selective toxin produced by the necrotrophic fungus Pyrenophora tritici-repentis. The molecular mechanisms associated with cell death in sensitive wheat cultivars following ToxA application are not well understood. To address this question, we used the Affymetrix GeneChip Wheat Genome Array to compare gene expression in a sensitive wheat cultivar possessing the Tsn1 gene with the insensitive wheat cv.

The Tsn1-ToxA interaction in the wheat-Stagonospora nodorum pathosystem parallels that of the wheat-tan spot system.

The wheat tan spot fungus (Pyrenophora tritici-repentis) produces a well-characterized host-selective toxin (HST) known as Ptr ToxA, which induces necrosis in genotypes that harbor the Tsn1 gene on chromosome 5B. In previous work, we showed that the Stagonospora nodorum isolate Sn2000 produces at least 2 HSTs (SnTox1 and SnToxA). Sensitivity to SnTox1 is governed by the Snn1 gene on chromosome 1B in wheat.

Emergence of a new disease as a result of interspecific virulence gene transfer.

New diseases of humans, animals and plants emerge regularly. Enhanced virulence on a new host can be facilitated by the acquisition of novel virulence factors. Interspecific gene transfer is known to be a source of such virulence factors in bacterial pathogens (often manifested as pathogenicity islands in the recipient organism) and it has been speculated that interspecific transfer of virulence factors may occur in fungal pathogens.

Role of the arginyl-glycyl-aspartic motif in the action of Ptr ToxA produced by Pyrenophora tritici-repentis.

A fundamental problem of plant science is to understand the biochemical basis of plant/pathogen interactions. The foliar disease tan spot of wheat (Triticum aestivum), caused by Pyrenophora tritici-repentis, involves Ptr ToxA, a proteinaceous host-selective toxin that causes host cell death. The fungal gene ToxA encodes a 17.