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

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.

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.


2008 ◽  
Vol 98 (5) ◽  
pp. 488-491 ◽  
Author(s):  
R. P. Oliver ◽  
M. Lord ◽  
K. Rybak ◽  
J. D. Faris ◽  
P. S. Solomon

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.


Author(s):  
Kazi A. Kader ◽  
Robert M. Hunger ◽  
Aswathy Sreedharan ◽  
Stephen M. Marek

AbstractIn recent years, tan spot of wheat caused by the fungus Pyrenophora tritici-repentis has become more prevalent in Oklahoma. Experiments were conducted to investigate the race structure, disease symptoms and genetic variability in P. tritici-repentis isolates collected from winter wheat over three decades. Race determination was conducted for 16 isolates based on expression of necrosis and/or chlorosis produced on wheat differentials. Variability in disease symptoms expressed by 12 isolates was determined on 13 hard red winter wheat cultivars grown in Oklahoma. In addition, genetic variability among 17 isolates was determined using amplified fragment length polymorphism-polymerase chain reaction (AFLP-PCR). All isolates except one (El Reno) were classified as race 1. Isolates varied widely in producing necrosis and/or chlorosis symptoms on wheat cultivars, but necrosis with a chlorotic halo was predominant (56.4%). AFLP-PCR analysis using 13 primer pairs produced a total of 494 alleles of which 285 were polymorphic. The overall genetic diversity among the isolates was 25.2%. Genetic relationships based on cluster analysis and principal component analysis showed only minor differences between isolates, and isolates did not form tight clusters or groups. The isolates of P. tritici-repentis were predominantly race 1; however, they produced a range of tan spot symptoms on wheat cultivars. The lack of distinct genetic grouping by the AFLP marker study indicates that the isolates used in this study likely originated from a single lineage.


2013 ◽  
Vol 103 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Dongwon Kim ◽  
Richard Jeannotte ◽  
Ruth Welti ◽  
William W. Bockus

Lipid profiles in wheat leaves and the effects of tan spot on the profiles were quantified by mass spectrometry. Inoculation with Pyrenophora tritici-repentis significantly reduced the amount of leaf lipids, including the major plastidic lipids monogalactosyldiacylglycerol (MGDG) and digalactosyldiacylglycerol (DGDG), which together accounted for 89% of the mass spectral signal of detected lipids in wheat leaves. Levels of these lipids in susceptible cultivars dropped much more quickly during infection than those in resistant cultivars. Furthermore, cultivars resistant or susceptible to tan spot displayed different lipid profiles; leaves of resistant cultivars had more MGDG and DGDG than susceptible ones, even in noninoculated plants. Lipid compositional data from leaves of 20 noninoculated winter wheat cultivars were regressed against an index of disease susceptibility and fitted with a linear model. This analysis demonstrated a significant relationship between resistance and levels of plastidic galactolipids and indicated that cultivars with high resistance to tan spot uniformly had more MGDG and DGDG than cultivars with high susceptibility. These findings suggest that lipid composition of wheat leaves may be a determining factor in the resistance response of cultivars to tan spot.


2018 ◽  
Vol 23 (10) ◽  
pp. 2086
Author(s):  
Fang Shiang Lim ◽  
Shih Keng Loong ◽  
Jing Jing Khoo ◽  
Kim Kee Tan ◽  
Nurhafiza Zainal ◽  
...  

AcknowledgmentsThis study was supported in parts by the research grants from University of Malaya, under the Research University Grants (RU016-2015) and (RU005-2017), and the Malaysia One Health University Network (MyOHUN) Seed Fund Award (MY/NCO/ACT/P001/SEEDFUND) provided by the United States Agency for International Development (USAID). 


Plant Disease ◽  
2021 ◽  
Author(s):  
Marwa Laribi ◽  
Alireza Akhavan ◽  
Sarrah M'Barek ◽  
Amor Yahyaoui ◽  
Stephen Ernest Strelkov ◽  
...  

Pyrenophora tritici-repentis (Ptr) causes tan spot, an important foliar disease of wheat. A collection of Ptr isolates from Tunisia, located in one of the main secondary centers of diversification of durum wheat, was tested for phenotypic race classification based on virulence on a host differential set, and for the presence of the necrotrophic effector (NE) genes ToxA, ToxB , and toxb by PCR analysis. While races 2, 4, 5, 6, 7, and 8 were identified according to their virulence phenotypes, PCR testing indicated the presence of ‘atypical’ isolates that induced necrosis on the wheat differential ‘Glenlea’, but lacked the expected ToxA gene, suggesting the involvement of other NEs in the Ptr/wheat interaction. Genetic diversity and the Ptr population structure were explored further by examining 59 Tunisian isolates and 35 isolates from Algeria, Azerbaijan, Canada, Iran, and Syria using 24 simple sequence repeat markers. Average genetic diversity, overall gene flow and percentage polymorphic loci were estimated as 0.58, 2.09 and 87%, respectively. Analysis of molecular variance showed that 81% of the genetic variance occurred within populations and 19% between populations. Cluster analysis by the unweighted pair group method indicated that ToxB- isolates grouped together and were distantly related to ToxB+ isolates. Based on Nei’s analysis, the global collection clustered into two distinct groups according to their region of origin. The results suggest that both geographic origin and the host-specificity imposed by different NEs can lead to differentiation among Ptr populations.


Pathogens ◽  
2018 ◽  
Vol 7 (3) ◽  
pp. 74 ◽  
Author(s):  
Jingwei Guo ◽  
Gongjun Shi ◽  
Zhaohui Liu

The fungus Pyrenophora tritici-repentis (Ptr) causes tan spot of wheat crops, which is an important disease worldwide. Based on the production of the three known necrotrophic effectors (NEs), the fungal isolates are classified into eight races with race 4 producing no known NEs. From a laboratory cross between 86–124 (race 2 carrying the ToxA gene for the production of Ptr ToxA) and DW5 (race 5 carrying the ToxB gene for the production of Ptr ToxB), we have obtained some Ptr isolates lacking both the ToxA and ToxB genes, which, by definition, should be classified as race 4. In this work, we characterized virulence of two of these isolates called B16 and B17 by inoculating them onto various common wheat (Triticum aestivum L.) and durum (T. turgidum L.) genotypes. It was found that the two isolates still caused disease on some genotypes of both common and durum wheat. Disease evaluations were also conducted in recombinant inbred line populations derived from two hard red winter wheat cultivars: Harry and Wesley. QTL mapping in this population revealed that three genomic regions were significantly associated with disease, which are different from the three known NE sensitivity loci. This result further indicates the existence of other NE-host sensitivity gene interactions in the wheat tan spot disease system.


2006 ◽  
Vol 96 (5) ◽  
pp. 542-548 ◽  
Author(s):  
Marcel Maymon ◽  
Aida Zveibil ◽  
Shimon Pivonia ◽  
Dror Minz ◽  
Stanley Freeman

Sixty-four isolates of Colletotrichum gloeosporioides were isolated from infected Limonium spp. cultivated in 12 different locations in Israel. All isolates were identified as belonging to the C. gloeosporioides complex by species-specific primers. Of these isolates, 46 were resistant to benomyl at 10 μg/ml and 18 were sensitive to this concentration of fungicide. Based on arbitrarily primed polymerase chain reaction of all isolates and internal transcribed spacer-1 sequence analyses of 12 selected isolates, the benomyl-resistant and -sensitive populations belong to two distinct genotypes. Sequence analyses of the β-tubulin genes, TUB1 and TUB2, of five sensitive and five resistant representative isolates of C. gloeosporioides from Limonium spp. revealed that the benomyl-resistant isolates had an alanine substitute instead of a glutamic acid at position 198 in TUB2. All data suggest that the resistant and sensitive genotypes are two independent and separate populations. Because all Limonium plant propagation material is imported from various geographic regions worldwide, and benomyl is not applied to this crop or for the control of Colletotrichum spp. in Israel, it is presumed that plants are bearing quiescent infections from the points of origin prior to arrival.


Plant Disease ◽  
2017 ◽  
Vol 101 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Anmin Wan ◽  
Kebede T. Muleta ◽  
Habtemariam Zegeye ◽  
Bekele Hundie ◽  
Michael O. Pumphrey ◽  
...  

Stripe rust, caused by Puccinia striiformis f. sp. tritici, is one of the most important diseases of wheat in Ethiopia. In total, 97 isolates were recovered from stripe rust samples collected in Ethiopia in 2013 and 2014. These isolates were tested on a set of 18 Yr single-gene differentials for characterization of races and 7 supplementary differentials for additional information of virulence. Of 18 P. striiformis f. sp. tritici races identified, the 5 most predominant races were PSTv-105 (21.7%), PSTv-106 (17.5%), PSTv-107 (11.3%), PSTv-76 (10.3%), and PSTv-41 (6.2%). High frequencies (>40%) were detected for virulence to resistance genes Yr1, Yr2, Yr6, Yr7, Yr8, Yr9, Yr17, Yr25, Yr27, Yr28, Yr31, Yr43, Yr44, YrExp2, and YrA. Low frequencies (<40%) were detected for virulence to Yr10, Yr24, Yr32, YrTr1, Hybrid 46, and Vilmorin 23. None of the isolates were virulent to Yr5, Yr15, YrSP, and YrTye. Among the six collection regions, Arsi Robe and Tiyo had the highest virulence diversities, followed by Bekoji, while Bale and Holeta had the lowest. Evaluation of 178 Ethiopian wheat cultivars and landraces with two of the Ethiopian races and three races from the United States indicated that the Ethiopian races were more virulent on the germplasm than the predominant races of the United States. Thirteen wheat cultivars or landraces that were resistant or moderately resistant to all five tested races should be useful for breeding wheat cultivars with resistance to stripe rust in both countries.


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