scholarly journals Emergence of Tan Spot Disease Caused by Toxigenic Pyrenophora tritici-repentis in Australia Is Not Associated with Increased Deployment of Toxin-Sensitive Cultivars

2008 ◽  
Vol 98 (5) ◽  
pp. 488-491 ◽  
Author(s):  
R. P. Oliver ◽  
M. Lord ◽  
K. Rybak ◽  
J. D. Faris ◽  
P. S. Solomon
Keyword(s):  
The United States ◽  
Tan Spot ◽  
Wheat Cultivars ◽  
Tillage Practices ◽  
Pyrenophora Tritici Repentis ◽  
South Wales ◽  
Glume Blotch ◽  
Wheat Gene ◽  
Serious Disease ◽  
Wheat Lines

The wheat disease tan (or yellow leaf) spot, caused by Pyrenophora tritici-repentis, was first described in the period 1934 to 1941 in Canada, India, and the United States. It was first noted in Australia in 1953 and only became a serious disease in the 1970s. The emergence of this disease has recently been linked to the acquisition by P. tritici-repentis of the ToxA gene from the wheat leaf and glume blotch pathogen, Stagonospora nodorum. ToxA encodes a host-specific toxin that interacts with the product of the wheat gene Tsn1. Interaction of ToxA with the dominant allele of Tsn1 causes host necrosis. P. tritici-repentis races lacking ToxA give minor indistinct lesions on wheat lines, whereas wheat lines expressing the recessive tsn1 are significantly less susceptible to the disease. Although the emergence and spread of tan spot had been attributed to the adoption of minimum tillage practices, we wished to test the alternative idea that the planting of Tsn1 wheat lines may have contributed to the establishment of the pathogen in Australia. To do this, wheat cultivars released in Australia from 1911 to 1986 were tested for their sensitivity to ToxA. Prior to 1941, 16% of wheat cultivars were ToxA-insensitive and hence, all other factors being equal, would be more resistant to the disease. Surprisingly, only one of the cultivars released since 1940 was ToxA insensitive, and the area planted to ToxA-insensitive cultivars varied from 0 to a maximum of only 14% in New South Wales. Thus, the majority of the cultivars were ToxA-sensitive both before and during the period of emergence and spread of the disease. We therefore conclude that the spread of P. tritici-repentis in Australia cannot be causally linked to the deployment of ToxA-sensitive cultivars.

scholarly journals Identification and Characterization of Novel Isolates of Pyrenophora tritici-repentis from Arkansas

Plant Disease ◽  
2010 ◽  
Vol 94 (2) ◽  
pp. 229-235 ◽  
Author(s):  
Shaukat Ali ◽  
Suraj Gurung ◽  
Tika B. Adhikari
Keyword(s):  
The United States ◽  
Tan Spot ◽  
Wheat Cultivars ◽  
Pyrenophora Tritici Repentis ◽  
Winter Wheat Cultivars ◽  
Race 1 ◽  
Preliminary Study ◽  
Polymerase Chain ◽  
Identification And Characterization

Tan spot, caused by Pyrenophora tritici-repentis, is an important foliar disease of wheat (Triticum aestivum) worldwide. In a preliminary study, P. tritici-repentis isolates from Arkansas were shown to vary in virulence relative to isolates from other regions of the United States. Therefore, the aim of the current study was to characterize both pathogenic and molecular variations in P. tritici-repentis isolates from Arkansas. The virulence of 93 isolates of P. tritici-repentis was evaluated by inoculating five differential wheat cultivars/lines. Based on virulence phenotypes, 63 isolates were classified as race 1, and 30 isolates were assigned to race 3. A subset of 42 isolates was selected for molecular characterization with the presence or absence of the ToxA and ToxB genes. The results showed that 36 isolates out of 42 tested by polymerase chain reaction (PCR) and Southern analysis lacked the ToxA and ToxB genes. Six isolates harboring the ToxA and ToxB genes induced necrosis and chlorosis on Glenlea and 6B365, respectively. Thirteen ToxA gene-deficient isolates also caused necrosis and chlorosis on Glenlea and 6B365, respectively; however, they did not fit current race classification. In contrast, the remaining 23 ToxA gene-deficient isolates did not cause necrosis, but induced chlorosis on 6B365, showing a disease profile for race 3. When the virulence of AR LonB2 (an isolate with unclassified race) was compared with known races 1, 3, and 5 of P. tritici-repentis on 20 winter wheat cultivars from Arkansas, the virulence phenotypes differed substantially. Taken together, the ToxA and ToxB gene-deficient isolates of P. tritici-repentis that induce necrosis and/or chlorosis may produce a novel toxin(s) on wheat.

scholarly journals A Novel Source of Resistance in Wheat to Pyrenophora tritici-repentis Race 1

Plant Disease ◽  
2008 ◽  
Vol 92 (1) ◽  
pp. 91-95 ◽  
Author(s):  
Sukhwinder Singh ◽  
William W. Bockus ◽  
Indu Sharma ◽  
Robert L. Bowden
Keyword(s):  
Great Plains ◽  
Recombinant Inbred Lines ◽  
The United States ◽  
Interval Mapping ◽  
Tan Spot ◽  
Sources Of Resistance ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Chromosome 5B ◽  
Race 1

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.

scholarly journals Isolate Virulence and Cultivar Response in the Winter Wheat: Pyrenophora tritici-repentis (Tan Spot) Pathosystem in Oklahoma

2021 ◽  
Vol 37 (4) ◽  
pp. 339-346
Author(s):  
Kazi A. Kader ◽  
Robert M. Hunger ◽  
Mark E. Payton
Keyword(s):  
Cluster Analysis ◽  
Leaf Area ◽  
Tan Spot ◽  
Wheat Cultivars ◽  
Cultivar Resistance ◽  
Wheat Varieties ◽  
Pyrenophora Tritici Repentis ◽  
Greenhouse Study ◽  
No Till ◽  
Increased Susceptibility

Prevalence of tan spot of wheat caused by the fungus Pyrenophora tritici-repentis has become more prevalent in Oklahoma as no-till cultivation in wheat has increased. Hence, developing wheat varieties resistant to tan spot has been emphasized, and selecting pathogen isolates to screen for resistance to this disease is critical. Twelve isolates of P. tritici-repentis were used to inoculate 11 wheat cultivars in a greenhouse study in splitplot experiments. Virulence of isolates and cultivar resistance were measured in percent leaf area infection for all possible isolate x cultivar interactions. Isolates differed significantly (P < 0.01) in virulence on wheat cultivars, and cultivars differed significantly in disease reaction to isolates. Increased virulence of isolates detected increased variability in cultivar response (percent leaf area infection) (r = 0.56, P < 0.05) while increased susceptibility in cultivars detected increased variance in virulence of the isolates (r = 0.76, P < 0.01). A significant isolate × cultivar interaction indicated specificity between isolates and cultivars, however, cluster analysis indicated low to moderate physiological specialization. Similarity in wheat cultivars in response to pathogen isolates also was determined by cluster analysis. The use of diverse isolates of the fungus would facilitate evaluation of resistance in wheat cultivars to tan spot.

scholarly journals Evaluation and Association Mapping of Resistance to Tan Spot and Stagonospora Nodorum Blotch in Adapted Winter Wheat Germplasm

Plant Disease ◽  
2015 ◽  
Vol 99 (10) ◽  
pp. 1333-1341 ◽  
Author(s):  
Zhaohui Liu ◽  
Ibrahim El-Basyoni ◽  
Gayan Kariyawasam ◽  
Guorong Zhang ◽  
Allan Fritz ◽  
...  
Keyword(s):  
United States ◽  
Winter Wheat ◽  
Association Mapping ◽  
Great Plains ◽  
The United States ◽  
Tan Spot ◽  
Stagonospora Nodorum ◽  
Northern Great Plains ◽  
Stagonospora Nodorum Blotch ◽  
Pyrenophora Tritici Repentis

Tan spot and Stagonospora nodorum blotch (SNB), often occurring together, are two economically significant diseases of wheat in the Northern Great Plains of the United States. They are caused by the fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively, both of which produce multiple necrotrophic effectors (NE) to cause disease. In this work, 120 hard red winter wheat (HRWW) cultivars or elite lines, mostly from the United States, were evaluated in the greenhouse for their reactions to the two diseases as well as NE produced by the two pathogens. One P. nodorum isolate (Sn4) and four Pyrenophora tritici-repentis isolates (Pti2, 331-9, DW5, and AR CrossB10) were used separately in the disease evaluations. NE sensitivity evaluation included ToxA, Ptr ToxB, SnTox1, and SnTox3. The numbers of lines that were rated highly resistant to individual isolates ranged from 11 (9%) to 30 (25%) but only six lines (5%) were highly resistant to all isolates, indicating limited sources of resistance to both diseases in the U.S. adapted HRWW germplasm. Sensitivity to ToxA was identified in 83 (69%) of the lines and significantly correlated with disease caused by Sn4 and Pti2, whereas sensitivity to other NE was present at much lower frequency and had no significant association with disease. As expected, association mapping located ToxA and SnTox3 sensitivity to chromosome arm 5BL and 5BS, respectively. A total of 24 potential quantitative trait loci was identified with −log (P value) > 3.0 on 12 chromosomes, some of which are novel. This work provides valuable information and tools for HRWW production and breeding in the Northern Great Plains.

Molecular mapping of resistance genes to tan spot [Pyrenophora tritici-repentis race 1] in synthetic wheat lines

2007 ◽  
Vol 114 (5) ◽  
pp. 855-862 ◽  
Author(s):  
W. Tadesse ◽  
M. Schmolke ◽  
S. L. K. Hsam ◽  
V. Mohler ◽  
G. Wenzel ◽  
...  
Keyword(s):  
Resistance Genes ◽  
Molecular Mapping ◽  
Tan Spot ◽  
Synthetic Wheat ◽  
Pyrenophora Tritici Repentis ◽  
Race 1 ◽  
Wheat Lines

Hybrid necrosis as a barrier to gene transfer in hexaploid winter wheat × triticale crosses

1998 ◽  
Vol 78 (2) ◽  
pp. 239-244 ◽  
Author(s):  
B. Bizimungu ◽  
J. Collin ◽  
A. Comeau ◽  
C.-A. St-Pierre
Keyword(s):  
Gene Transfer ◽  
Winter Wheat ◽  
Wheat Cultivars ◽  
Hybrid Necrosis ◽  
Cross Direction ◽  
Wheat Gene ◽  
Special Value ◽  
Winter Wheat Cultivars ◽  
Main Barrier ◽  
Wheat Lines

An interspecific wheat × triticale hybridization program was initiated with the scope of widening and improving the winter wheat gene pool. However, progress was hampered by severe necrosis that caused the death of F1 hybrids from crosses between the most winterhardy wheat and triticale cultivars. This paper describes hybrid necrosis as the main barrier to gene transfer between winter wheat cultivars Borden, Augusta and Ruby, and hexaploid winter triticales OAC Wintri and K9-6. Crosses with tester lines revealed that the three winter wheats were carriers of the necrotic Ne2 allele. High temperature (30 °C) treatment until heading stage permitted to only partially circumvent the problem. A study of cross direction effects at the backcross level showed that the conventional method (F1 × wheat) was more efficient for plant recovery, but plants produced by the alternative backcross system (wheat × F1) were more self-fertile. Within the most winterhardy germplasm, hybrid necrosis is a major problem for transferring genes between winter wheat and triticale. The use of non-necrotic winter wheat lines such as MC11N, a local winter wheat selection, may have a special value as a bridge to circumvent the necrosis problem. Key words: Hybrid necrosis, Ne genes, wheat × triticale hybrids, cross direction

scholarly journals Role of Host Sensitivity to Ptr ToxA in Development of Tan Spot of Wheat

2003 ◽  
Vol 93 (4) ◽  
pp. 397-401 ◽  
Author(s):  
T. L. Friesen ◽  
S. Ali ◽  
S. Kianian ◽  
L. J. Francl ◽  
J. B. Rasmussen
Keyword(s):  
Genetic Variance ◽  
Dominant Gene ◽  
Tan Spot ◽  
Wild Type ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Recombinant Inbred Population ◽  
Race 2 ◽  
Wheat Lines

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.

scholarly journals A Two-Step Molecular Detection Method for Pyrenophora tritici-repentis Isolates Insensitive to QoI Fungicides

Plant Disease ◽  
2011 ◽  
Vol 95 (12) ◽  
pp. 1558-1564 ◽  
Author(s):  
Jaimin S. Patel ◽  
Steven W. Meinhardt ◽  
Helge Sierotzki ◽  
Gerd Stammler ◽  
Neil C. Gudmestad ◽  
...  
Keyword(s):  
Genomic Dna ◽  
Molecular Detection ◽  
Detection Method ◽  
The United States ◽  
Tan Spot ◽  
Complex Iii ◽  
Cyt B ◽  
Qoi Fungicides ◽  
Pyrenophora Tritici Repentis ◽  
Cyt B Gene

Tan spot, caused by Pyrenophora tritici-repentis, is an important disease of wheat worldwide. To manage tan spot, quinone outside inhibitor (QoI) fungicides such as azoxystrobin and pyraclostrobin have been applied in many countries. QoI fungicides target the cytochrome b (cyt b) site in complex III of mitochondria and, thus, pose a serious risk for resistance development. The resistance mechanism to QoI fungicides is mainly due to point mutations in the cyt b gene. The objective of this study was to develop a molecular detection method for the four currently known mutations responsible for shifts in sensitivity toward QoI fungicides in P. tritici-repentis. Twelve specific primers were designed based on sequences from the National Center for Biotechnology Information accessions AAXI01000704 and DQ919068 and used to generate a fragment of the cyt b gene which possesses four known single-nucleotide polymorphisms (SNPs). These mutant clones served as positive controls because QoI-insensitive and -reduced-sensitive isolates of P. tritici-repentis have not yet been reported in the United States. The partial cyt b gene clones were sequenced to identify the SNPs at sites G143A and F129L. Genomic DNA of the mutated partial cyt b gene clones and the European QoI-insensitive and -reduced-sensitive isolates of P. tritici-repentis possessing G143A (GCT) and F129L (TTA, TTG, and CTC) mutations were amplified by polymerase chain reaction (PCR) using two specific primer pairs and were further digested with three specific restriction enzymes (BsaJI, Fnu4HI, and MnlI). The results of the digested PCR product from genomic DNA of known QoI-insensitive and -reduced-sensitive isolates of P. tritici-repentis had DNA bands consistent with the mutation GCT at G143A and the mutations TTA, TTG, and CTC at F129L. The amplified region at the F129 site also had 99% sequence similarity with P. teres, the net blotch pathogen of barley. To validate mutations, we further tested two isolates of P. teres known to have reduced sensitivity to QoI fungicides possessing the mutations TTA and CTC at F129L. After PCR amplification and restriction digestion, DNA bands identical to those observed for the partial cyt b mutant clones were detected. These results suggest that this newly developed two-step molecular detection method is rapid, robust, and specific to monitor QoI-insensitive and -reduce-dsensitive isolates of P. tritici-repentis.

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