The variability of a Pyrenophora tritici-repentis population as revealed by inter-retrotransposon amplified polymorphism with regard to the Ptr ToxA gene.

2010 ◽  
Vol 61 (2) ◽  
pp. 125-138 ◽  
Author(s):  
Leona Leišová-Svobodová ◽  
Alena Hanzalová ◽  
Ladislav Kučera
Plant Disease ◽  
2008 ◽  
Vol 92 (1) ◽  
pp. 91-95 ◽  
Author(s):  
Sukhwinder Singh ◽  
William W. Bockus ◽  
Indu Sharma ◽  
Robert L. Bowden

Tan spot, caused by the fungus Pyrenophora tritici-repentis, causes serious yield losses in wheat (Triticum aestivum) and many other grasses. Race 1 of the fungus, which produces the necrosis toxin Ptr ToxA and the chlorosis toxin Ptr ToxC, is the most prevalent race in the Great Plains of the United States. Wheat genotypes with useful levels of resistance to race 1 have been deployed, but this resistance reduces damage by only 50 to 75%. Therefore, new sources of resistance to P. tritici-repentis are needed. Recombinant inbred lines developed from a cross between the Indian spring wheat cvs. WH542 (resistant) and HD29 (moderately susceptible) were evaluated for reaction to race 1 of the fungus. Composite interval mapping revealed quantitative trait loci (QTL) on the short arm of chromosome 3A explaining 23% of the phenotypic variation, and the long arm of chromosome 5B explaining 27% of the variation. Both resistance alleles were contributed by the WH542 parent. The QTL on 5BL is probably tsn1, which was described previously. The 3AS QTL (QTs.ksu-3AS) on 3AS is a novel QTL for resistance to P. tritici-repentis race 1. The QTL region is located in the most distal bin of chromosome 3AS in a 2.2-centimorgan marker interval. Flanking markers Xbarc45 and Xbarc86 are suitable for marker-assisted selection for tan spot resistance.


2021 ◽  
Author(s):  
Janis Kaneps ◽  
◽  
Biruta Bankina ◽  
Inga Moročko-Bičevska ◽  

Pyrenophora tritici-repentis is a major wheat pathogen in all wheat (Triticum spp.) growing areas worldwide. Up to date, eight P. tritici-repentis races have been described based on chlorosis, necrosis, or both symptoms caused on race differential wheat genotypes: ‘Glenlea’, 6B662, 6B365, and ‘Salamouni’. Symptom development on differential genotypes depends on the interaction of the pathogen’s necrotrophic effectors named Ptr ToxA, Ptr ToxB, and Ptr ToxC with host susceptibility genes. Ptr ToxA is encoded by the single copy gene ToxA and induces necrosis on sensitive wheat cultivars. Ptr ToxB causes chlorosis and is encoded by the multicopy gene ToxB. The Ptr ToxC is the non-proteinaceous, polar, low molecular mass molecule that also induces chlorosis, but up to date, the gene encoding this toxin is unknown. Races producing Ptr ToxA are predominant in the global Ptr population. There are several reports about new putative races of P. tritici-repentis that do not conform with the current race system, so further research is required. This study aims to collect and systematise available information about the virulence and races of P. tritici-repentis.


2000 ◽  
Vol 13 (4) ◽  
pp. 456-464 ◽  
Author(s):  
Robert P. Tuori ◽  
Thomas J. Wolpert ◽  
Lynda M. Ciuffetti

Ptr ToxA, a proteinaceous host-selective toxin (HST) produced by the fungus Pyrenophora tritici-repentis, was expressed in Escherichia coli and purified as a polyhistidine-tagged, fusion protein (NC-FP). NC-FP, consisting of both the N and C domains of the ToxA open reading frame (ORF), is produced as an insoluble protein in E. coli at approximately 10 to 16 mg per liter of culture. Following in vitro refolding, NC-FP elicits cultivar-specific necrosis in wheat, with a specific activity similar to that of native Ptr ToxA. A fusion protein consisting of only the C domain has approximately 10 to 20% of the activity of native Ptr ToxA. These data suggest that (i) the N domain is important for maximal activity of Ptr ToxA, (ii) the N domain does not function to eliminate activity of the protoxin, and (iii) post-translational modifications of Ptr ToxA are not essential for activity. A C domain construct with a cysteine residue mutated to glycine is inactive. This, plus the observation that toxin activity is sensitive to reducing agents, provides evidence that the two cysteine residues in Ptr ToxA are involved in a disulfide bond that is essential for activity. The heterologous expression of Ptr ToxA provides a valuable tool for addressing a number of issues such as receptor binding studies, structure/function studies, and screening wheat cultivars for disease resistance.


2010 ◽  
Vol 187 (4) ◽  
pp. 911-919 ◽  
Author(s):  
Lynda M. Ciuffetti ◽  
Viola A. Manning ◽  
Iovanna Pandelova ◽  
Melania Figueroa Betts ◽  
J. Patrick Martinez

2003 ◽  
Vol 93 (4) ◽  
pp. 397-401 ◽  
Author(s):  
T. L. Friesen ◽  
S. Ali ◽  
S. Kianian ◽  
L. J. Francl ◽  
J. B. Rasmussen

Pyrenophora tritici-repentis race 2 produces Ptr ToxA, a host-selective toxin previously described as a pathogenicity factor for tan spot on wheat. The objective of this research was to evaluate the role of host sensitivity to toxin, conditioned by a single dominant gene on chromosome 5BL, in the disease development by race 2. An F2-derived F6 recombinant inbred population of 108 wheat lines, produced from crosses of toxin-sensitive, disease-susceptible cv. Kulm with the toxin-insensitive, disease-resistant cv. Erik segregated 1:1 for toxin reaction. However, the population was skewed toward resistance to race 2 of the fungus. Toxin reaction accounted for 24.4% of the genetic variance for disease. Heritability estimates suggested the presence of four to five genes that influence disease reaction in the population. Toxin-insensitive mutants, previously derived Kulm, were susceptible to race 2, although disease developed more slowly on the mutants than it did on the wild-type Kulm. The data indicate that sensitivity to Ptr ToxA influences disease severity in some host genotypes without defining susceptibility.


2005 ◽  
Vol 17 (11) ◽  
pp. 3190-3202 ◽  
Author(s):  
Ganapathy N. Sarma ◽  
Viola A. Manning ◽  
Lynda M. Ciuffetti ◽  
P. Andrew Karplus

2019 ◽  
Vol 22 (8) ◽  
pp. 978-986 ◽  
Author(s):  
A. М. Kokhmetova ◽  
Sh. Ali ◽  
Z. Sapakhova ◽  
M. N. Atishova

Pyrenophora tritici-repentis(Ptr) is the causative agent of tan spot, one of the yield limiting diseases of wheat, rapidly increasing in wheat growing countries including Kazakhstan. The aim of this study was the identifcation of wheat genotypes with resistance to Ptr race 1 and race 5 and their host­selective effectors (toxins) Ptr ToxA and Ptr ToxB. A common wheat collection of 41 accessions (38 experimental and 3 controls) was characterized using the molecular markersXfcp623andXBE444541, diagnostic for theTsn1andTsc2genes conferring sensitivity to fungal toxins. The coincidence of the markerXBE444541with resistance to race 5 was 92.11 %, and with Ptr ToxB, 97.37 %. Genotyping results using the markerXfcp623confrmed the expected response to Ptr ToxA; the presence/absence of the markerXfcp623completely (100 %) coincided with sensitivity/resistance to race 1 and Ptr ToxA. This demonstrates the reliability of the diagnostic markerXfcp623for identifying wheat genotypes with resistance to the fungus and insensitivity to Ptr ToxA. The study of the reaction of wheat germplasm to the fungal inoculation and toxin infltration showed that out of 38 genotypes analyzed 30 (78 %) exhibited resistance to both race 1 and race 5, and insensitivity to toxins Ptr ToxA and ToxB. Of most signifcant interest are eight wheat genotypes that showed resistance/insensitivity both to the two races and two toxins. The results of phenotyping were reconfrmed by the molecular markers used in this study. Sensitivity to Ptr ToxB is not always correlated with susceptibility to race 5 and is dependent on the host’s genetic background of the wheat genotype, i. e. on a specifc wheat genotype. The results of the study are of interest for increasing the efciency of breeding based on the elimination of the genotypes with the dominant allelesTsn1andTsc2sensitive to the toxins Ptr ToxA and ToxB. The genotypes identifed will be used in wheat breeding for resistance to tan spot.


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