Reaction of Ptr ToxA-Insensitive Wheat Mutants to <i>Pyrenophora tritici-repentis</i> Race 1

Friesen, Timothy L.; Rasmussen, J. B.; Kwon, C. Y.; Francl, L. J.; Meinhardt, S. W.

doi:10.1094/phyto.2002.92.1.38

Cited by 47 publications

(35 citation statements)

References 16 publications

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“…Similarly, 25% of durum and 15% of hard red spring wheat lines were found to be susceptible to the fungus and insensitive to the Ptr ToxA . Furthermore, our results were in agreement a For tan spot reaction, plants were rated for disease reaction 8 days after inoculation with Pyrenophora tritici-repentis (PTR) race 1 according to the 1 to 5 lesion type rating scale (Friesen et al, 2002), where 2 = resistant (R) and > 2 = susceptible (S) b Reaction to Ptr ToxA was scored as S and I (Lamari and Bernier, 1989). S and I stand for sensitive and insensitive, respectively For Stagonospora nodorum blotch (SNB) reaction, seedlings were rated for disease reaction 7 days after inoculation based on a 0 to 5 scale (Liu et al 2004), where 2 were considered as resistant (R) and > 2 were susceptible (S) a D.S.…”

Section: Discussionsupporting

confidence: 83%

“…Pyrenophora tritici-repentis toxins are found to be associated with the fungal pathogenicity factor or virulence factor (Friesen et al 2002(Friesen et al , 2006. The Ptr ToxA toxin is produced by PTR races 1, 2, 7, and 8 and has been suggested to be a rapid tool for screening wheat germplasm for resistance to the necrosis component of the disease (Singh et al 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Meinhardt, Department of Plant Pathology, NDSU, Fargo, ND. The 164 wheat genotypes were evaluated against Ptr ToxA as described previously (Friesen et al 2002;Singh et al 2006). Approximately, 10 ll of Ptr ToxA (10 lg ml À1 ) was infiltrated into the second leaf of wheat using a 1-ml syringe without a needle 14 days after planting.…”

Section: Screening For Tan Spotmentioning

confidence: 99%

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Resistance to multiple leaf spot diseases in wheat

et al. 2007

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Tan spot (TS), Stagonospora nodorum blotch (SNB), and Septoria tritici blotch (STB) are three major leaf spot diseases of wheat worldwide. Host plant resistance (HPR) is one of the main components in the management of these diseases in wheat. The objective of this study was to identify new sources of resistance to TS (races 1 and 5), SNB, and STB. A total of 164 wheat genotypes developed by the International Maize and Wheat Improvement Center (CIMMYT), Mexico were individually evaluated for TS, SNB and STB in spring and fall of 2006 in the greenhouse. Two experiments were conducted in a randomized complete block design with three replicates. Each replicate consisted of 164 wheat genotypes planted in cones with three seedlings/ genotype in each cone and disease reaction was assessed for each race or pathogen at the two-to three-leaf stage. Based on the disease reactions, three wheat genotypes were resistant to both TS and SNB, while 13 genotypes were resistant to TS and STB. Similarly, 13 genotypes were resistant to both SNB and STB. In addition, four wheat genotypes were highly resistant to TS, SNB, and STB. These results suggest that the resistant genotypes identified in this study possess high levels of resistance to multiple leaf spot diseases and could be valuable sources for wheat improvement programs.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Screening For Tan Spotmentioning

confidence: 99%

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Resistance to multiple leaf spot diseases in wheat

et al. 2007

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“…To confirm further that the S/TPK-NBS-LRR gene was Tsn1, we sequenced the gene from the remaining 10 mutants along with 3 mutants previously developed in the hexaploid variety Kulm (16), and analysis revealed that all 13 harbored mutations consisting of missense, nonsense, and splice site mutations ( Table 1). The splice site mutations occurred in mutants LDNems230 and Kems103, and they were further validated by RT-PCR ( Fig.…”

Section: Resultsmentioning

confidence: 99%

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

Faris

Zhang²,

Lu³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

473

405

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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. The effector ToxA is produced by both pathogens, and sensitivity to ToxA is governed by the Tsn1 gene on wheat chromosome arm 5BL. Here, we report the cloning of Tsn1 , which was found to have disease resistance gene-like features, including S/TPK and NBS-LRR domains. Mutagenesis revealed that all three domains are required for ToxA sensitivity, and hence disease susceptibility. Tsn1 is unique to ToxA-sensitive genotypes, and insensitive genotypes are null. Sequencing and phylogenetic analysis indicated that Tsn1 arose in the B-genome diploid progenitor of polyploid wheat through a gene-fusion event that gave rise to its unique structure. Although Tsn1 is necessary to mediate ToxA recognition, yeast two-hybrid experiments suggested that the Tsn1 protein does not interact directly with ToxA. Tsn1 transcription is tightly regulated by the circadian clock and light, providing further evidence that Tsn1 -ToxA interactions are associated with photosynthesis pathways. This work suggests that these necrotrophic pathogens may thrive by subverting the resistance mechanisms acquired by plants to combat other pathogens.

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“…So far, the isolates from wheat and alternative host plants have been grouped into eight races [ 2,[9][10][11] and race 1 was the most prevalent race observed in Africa, Asia, Europe, North and South America [2,9,[11][12][13][14][15]. Further, P. tritici-repentis produces three host-selective toxins, Ptr ToxA, Ptr ToxB, and Ptr ToxC, which are associated with necrosis and chlorosis symptoms in toxins sensitive wheat genotypes [11,[16][17][18]. At present gene-specific molecular markers are available for Ptr ToxA (associated with necrosis symptom) and Ptr ToxB (chlorosis) and can be used to determine if an isolate carries these genes.…”

Section: Introductionmentioning

confidence: 99%

Race Diversity of Pyrenophora tritici-repentis in South Dakota and Response of Predominant Wheat Cultivars to Tan Spot

Abdullah¹,

Sk²,

Ali³

2017

J Plant Pathol Microbiol

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The fungus Pyrenophora tritici-repentis (Ptr) causing tan spot (TS) is an important pathogen of wheat in the US Northern-Great-Plains. Knowledge of physiological variation in the pathogen population is essential in the development of durable TS resistant cultivars. Eight Ptr races have been identified based on three host selective toxins (Ptr ToxA/Ptr ToxB/Ptr ToxC), which are associated with necrosis and chlorosis symptoms. The information about Ptr race structure and reaction of wheat cultivars grown in SD to tan spot is scarcely available. In this study, 569 isolates of Ptr collected from wheat were genotyped for Ptr ToxA and Ptr ToxB genes and a subset of 134 isolates were evaluated for their race identity on a wheat differential set. Ptr ToxA and Ptr ToxB genes were amplified in 89.6% and 0.4% isolates, respectively. The remaining 57 (10%) isolates lacked both toxins genes. The characterization of 134 isolates exhibited diverse race structure with 74.6%, 18.7%, 1.49% , and <1% isolates categorized as race 1, 4, 5, and 2, respectively. Another six (4.5%) isolates behaved like race 2 but lacked Ptr ToxA gene, hence could not fit under the currently known eight races. Our results determine the diversity of Ptr population that exists in SD and establish the presence of race 5 in SD for the first time. Since races 1 and 5 are most prevalent in the region, we screened 45 most predominant wheat cultivars against these races and Ptr ToxA. We observed eleven cultivars resistant or moderately resistant to both races, however, seven spring wheat cultivars showed susceptibility to both races 1 and 5. Continued cultivation of wheat cultivars susceptible to both races could play a role in the establishment and development of new races. Continuous germplasm enhancement and periodically monitoring Ptr population can help in better TS management.

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Reaction of Ptr ToxA-Insensitive Wheat Mutants to Pyrenophora tritici-repentis Race 1

Cited by 47 publications

References 16 publications

Resistance to multiple leaf spot diseases in wheat

Resistance to multiple leaf spot diseases in wheat

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

Race Diversity of Pyrenophora tritici-repentis in South Dakota and Response of Predominant Wheat Cultivars to Tan Spot

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