scholarly journals ToxA Is Present in the U.S. Bipolaris sorokiniana Population and Is a Significant Virulence Factor on Wheat Harboring Tsn1

Plant Disease ◽  
2018 ◽  
Vol 102 (12) ◽  
pp. 2446-2452 ◽  
Author(s):  
T. L. Friesen ◽  
D. J. Holmes ◽  
R. L. Bowden ◽  
J. D. Faris
Keyword(s):  
Winter Wheat ◽  
Bipolaris Sorokiniana ◽  
Selective Advantage ◽  
The United States ◽  
Tan Spot ◽  
Single Spore ◽  
Pyrenophora Tritici Repentis ◽  
Culture Filtrates ◽  
Parastagonospora Nodorum ◽  
Mutant Lines

ToxA, a necrotrophic effector originally identified from the tan spot fungus Pyrenophora tritici-repentis in 1987, was subsequently identified from Parastagonospora nodorum in 2006. More recently, the ToxA gene was identified in the spot blotch fungus Bipolaris sorokiniana in Australia. Here we show that the ToxA gene is also present in the B. sorokiniana population in the winter wheat region of southcentral Texas. Leaves from ‘Duster’ wheat showing strong necrotic lesions were collected in Castroville, TX. Fifteen single-spore isolates were collected from separate lesions, and 13 of them harbored the BsToxA gene and secreted ToxA in culture based on sensitivity of BG261, the differential line containing the dominant ToxA sensitivity gene, Tsn1. Four isolates harboring BsToxA and one deficient in BsToxA were used to infiltrate two wheat lines harboring Tsn1 as well as their corresponding tsn1 mutant lines. Culture filtrates of the isolate lacking BsToxA did not induce necrosis on any of the lines. Culture filtrates of the four BsToxA-containing isolates induced necrosis on the wild type (Tsn1) lines but not on the corresponding tsn1 mutant lines. Sensitivity to these culture filtrates also mapped to the previously identified location for Tsn1 in the winter wheat mapping population Arina × Forno. Inoculation of one of these ToxA-producing isolates on the same population showed that the Tsn1 locus accounted for 24.4% of the disease variation. All 13 isolates harbored the same BsToxA nucleotide sequence, which was identical to one of the two haplotypes previously identified in Australia. Sensitivity to ToxA is prevalent in popular hard winter wheat cultivars in the central and southcentral winter wheat regions of the United States, showing the potential of a selective advantage for B. sorokiniana isolates that harbor the ToxA gene.

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.

scholarly journals Parastagonospora nodorum and Related Species in Western Canada: Genetic Variability and Effector Genes

2020 ◽  
Vol 110 (12) ◽  
pp. 1946-1958
Author(s):  
Mohamed Hafez ◽  
Ryan Gourlie ◽  
Therese Despins ◽  
Thomas K. Turkington ◽  
Timothy L. Friesen ◽  
...  
Keyword(s):  
Evolutionary Relationship ◽  
Haplotype Network ◽  
Bipolaris Sorokiniana ◽  
Western Canada ◽  
Pyrenophora Tritici Repentis ◽  
Septoria Nodorum Blotch ◽  
Effector Genes ◽  
Parastagonospora Nodorum ◽  
Almost All ◽  
Necrotrophic Effectors

Parastagonospora nodorum is an important fungal pathogen that causes Septoria nodorum blotch (SNB) in wheat. This pathogen produces several necrotrophic effectors that act as virulence factors; three have been cloned, SnToxA, SnTox1, and SnTox3. In this study, P. nodorum and its sister species P. avenaria f. tritici (Pat1) were isolated from wheat node and grain samples collected from distanced sites in western Canada during 2018. The presence of effector genes and associated haplotypes were determined by PCR and sequence analysis. An internal transcribed spacer-restriction fragment length polymorphism test was developed to distinguish between leaf spotting pathogens (P. nodorum, Pat1, Pyrenophora tritici-repentis, and Bipolaris sorokiniana). P. nodorum was mainly recovered from wheat nodes and to a lesser extent from the grains, while Pat1 was exclusively isolated from grain samples. The effector genes were present in almost all P. nodorum isolates, with the ToxA haplotype 5 (H5) being most prevalent, while a novel ToxA haplotype (denoted here H21) is reported for the first time. In Pat1, only combinations of SnTox1 and SnTox3 genes were present. A ToxA haplotype network was also constructed to assess the evolutionary relationship among globally found haplotypes to date. Finally, cultivars representing wheat development in Canada for the last century were tested for sensitivity to Sn-effectors and to the presence of Tsn1, the ToxA sensitivity gene. Of tested cultivars, 32.9 and 56.9% were sensitive to SnTox1 and SnTox3, respectively, and Tsn1 was present in 59% of the cultivars. In conclusion, P. nodorum and Pat1 were prevalent wheat pathogens in Canada with a potential tissue-specific colonization capacity, while producing necrotrophic effectors to which wheat is sensitive.

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 Genetic Control of Resistance to Tan Necrosis Induced by Pyrenophora tritici-repentis, Races 1 and 2, in Spring and Winter Wheat Genotypes

2005 ◽  
Vol 95 (2) ◽  
pp. 172-177 ◽  
Author(s):  
P. K. Singh ◽  
G. R. Hughes
Keyword(s):  
Winter Wheat ◽  
Genetic Control ◽  
Recessive Gene ◽  
Tan Spot ◽  
Wheat Genotypes ◽  
Resistant Cultivars ◽  
Pyrenophora Tritici Repentis ◽  
Lesion Type ◽  
Race 1 ◽  
Race 2

The symptoms of tan spot of wheat, caused by Pyrenophora triticirepentis, include a tan necrosis component and an extensive chlorosis component. Since tan spot has become the major component of the leafspotting disease complex of wheat in western Canada, the need for resistant cultivars has increased. This study was conducted to determine whether the resistance to tan spot found in a diverse set of spring and winter wheat genotypes was due to resistance genes not previously reported. The genetic control of resistance to necrosis induced by P. triticirepentis race 1 and race 2 was determined, under controlled environmental conditions, for spring wheat genotypes Erik and 86ISMN 2137 and winter wheat genotypes Hadden, Red Chief, and 6B-365. Plants were inoculated at the two-leaf stage and disease reaction was assessed based on lesion type. Tests of the F1 and F2 generations, and of F2:3 and F2:8 families, indicated that one recessive gene controlled resistance to the necrosis component of tan spot caused by both race 1 and race 2 in each cross studied. Lack of segregation in crosses between the resistant cultivars indicated that the resistance gene was the same in all of the cultivars.

scholarly journals Population Race Structure of Pyrenophora tritici-repentis Prevalent on Wheat and Noncereal Grasses in the Great Plains

Plant Disease ◽  
2003 ◽  
Vol 87 (4) ◽  
pp. 418-422 ◽  
Author(s):  
Shaukat Ali ◽  
Leonard J. Francl
Keyword(s):  
Great Plains ◽  
Durable Resistance ◽  
First Record ◽  
Tan Spot ◽  
Single Spore ◽  
Smooth Bromegrass ◽  
Barnyard Grass ◽  
Disease Epidemiology ◽  
Pyrenophora Tritici Repentis ◽  
Slender Wheatgrass

The fungus Pyrenophora tritici-repentis, cause of tan spot of wheat, is an important foliar pathogen worldwide. Genetic variation in the fungal population prevalent in the Great Plains was studied by analysis of 270 single-spore isolates of P. tritici-repentis recovered from wheat, durum, and 10 noncereal grasses: Alti wild rye, barnyard grass, crested wheatgrass, intermediate wheatgrass, needle and thread grass, quackgrass, smooth bromegrass, sand reedgrass, slender wheatgrass, and wild barley. The isolates were grouped into five known races based on necrosis and/or chlorosis induction on standard differentials with two additional wheat genotypes ND495 and M-3. The isolates recovered from wheat were races 1, 2, and 4, while those from durum were races 1 and 5. Isolates from noncereal grasses were all race 4, except for the recovery of two isolates of race 1 from smooth bromegrass. Race 3 was not found in this study. This is the first record of barnyard grass and slender wheatgrass as alternative hosts for P. tritici-repentis. The recovery from noncereal grasses suggests that the fungus has a fairly wide host range; however, predominance of a race that is avirulent on wheat on these grasses tends to eliminate their significance in the disease epidemiology of wheat. The results indicate that P. tritici-repentis has a diverse population on wheat and noncereal grasses. For durable resistance, wheat lines should be tested against all virulent races found in the field.

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.

Genome-wide association mapping of tan spot resistance (Pyrenophora tritici-repentis) in European winter wheat

2014 ◽  
Vol 34 (2) ◽  
pp. 363-371 ◽  
Author(s):  
Sonja Kollers ◽  
Bernd Rodemann ◽  
Jie Ling ◽  
Viktor Korzun ◽  
Erhard Ebmeyer ◽  
...  
Keyword(s):  
Winter Wheat ◽  
Association Mapping ◽  
Tan Spot ◽  
Genome Wide Association ◽  
Pyrenophora Tritici Repentis ◽  
Genome Wide ◽  
European Winter Wheat

scholarly journals New Insights into the Roles of Host Gene-Necrotrophic Effector Interactions in Governing Susceptibility of Durum Wheat to Tan Spot and Septoria nodorum Blotch

2016 ◽  
Vol 6 (12) ◽  
pp. 4139-4150 ◽  
Author(s):  
Simerjot K Virdi ◽  
Zhaohui Liu ◽  
Megan E Overlander ◽  
Zengcui Zhang ◽  
Steven S Xu ◽  
...  
Keyword(s):  
Durum Wheat ◽  
Common Wheat ◽  
Tan Spot ◽  
Septoria Nodorum ◽  
Pyrenophora Tritici Repentis ◽  
Septoria Nodorum Blotch ◽  
Necrotrophic Fungi ◽  
Host Genetic ◽  
Parastagonospora Nodorum ◽  
Necrotrophic Effector

Abstract Tan spot and Septoria nodorum blotch (SNB) are important diseases of wheat caused by the necrotrophic fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively. The P. tritici-repentis necrotrophic effector (NE) Ptr ToxB causes tan spot when recognized by the Tsc2 gene. The NE ToxA is produced by both pathogens and has been associated with the development of both tan spot and SNB when recognized by the wheat Tsn1 gene. Most work to study these interactions has been conducted in common wheat, but little has been done in durum wheat. Here, quantitative trait loci (QTL) analysis of a segregating biparental population indicated that the Tsc2-Ptr ToxB interaction plays a prominent role in the development of tan spot in durum. However, analysis of two biparental populations indicated that the Tsn1-ToxA interaction was not associated with the development of tan spot, but was strongly associated with the development of SNB. Pa. nodorum expressed ToxA at high levels in infected Tsn1 plants, whereas ToxA expression in P. tritici-repentis was barely detectable, suggesting that the differences in disease levels associated with the Tsn1-ToxA interaction were due to differences in pathogen expression of ToxA. These and previous results together indicate that: (1) the effects of Tsn1-ToxA on tan spot in common wheat can range from nonsignificant to highly significant depending on the host genetic background; (2) Tsn1-ToxA is not a significant factor for tan spot development in durum wheat; and (3) Tsn1-ToxA plays a major role in SNB development in both common and durum wheat. Durum and common wheat breeders alike should strive to remove both Tsc2 and Tsn1 from their materials to achieve disease resistance.

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.

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.

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