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

Author(s):  
Abdullah S ◽  
Sehgal SK ◽  
Ali S
2021 ◽  
Vol 37 (4) ◽  
pp. 339-346
Author(s):  
Kazi A. Kader ◽  
Robert M. Hunger ◽  
Mark E. Payton

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.


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.


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.


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.


2015 ◽  
Vol 28 (10) ◽  
pp. 1082-1090 ◽  
Author(s):  
Melania Figueroa ◽  
Viola A. Manning ◽  
Iovanna Pandelova ◽  
Lynda M. Ciuffetti

The necrotrophic fungus Pyrenophora tritici-repentis is responsible for the disease tan spot of wheat. Ptr ToxB (ToxB), a proteinaceous host-selective toxin, is one of the effectors secreted by P. tritici-repentis. ToxB induces chlorosis in toxin-sensitive wheat cultivars and displays characteristics common to apoplastic effectors. We addressed the hypothesis that ToxB exerts its activity extracellularly. Our data indicate that hydraulic pressure applied in the apoplast following ToxB infiltration can displace ToxB-induced symptoms. In addition, treatment with a proteolytic cocktail following toxin infiltration results in reduction of symptom development and indicates that ToxB requires at least 8 h in planta to induce maximum symptom development. In vitro assays demonstrate that apoplastic fluids extracted from toxin-sensitive and -insensitive wheat cultivars cannot degrade ToxB. Additionally, ToxB can be reisolated from apoplastic fluid after toxin infiltration. Furthermore, localization studies of fluorescently labeled ToxB indicate that the toxin remains in the apoplast in toxin-sensitive and -insensitive wheat cultivars. Our findings support the hypothesis that ToxB acts as an extracellular effector.


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.


2021 ◽  
Vol 74 (1) ◽  
Author(s):  
Sean Weith ◽  
Hayley J. Ridgway ◽  
E. Eirian Jones

Tan spot, caused by Pyrenophora tritici-repentis (Ptr), is an important disease of wheat worldwide, and an emerging issue in New Zealand. The pathogen produces host-specific toxins which interact with the wheat host sensitivity loci. Identification of the prevalence of the toxin encoding genes in the local population, and the susceptibility of commonly grown wheat cultivars to Ptr will aid selection of wheat cultivars to reduce disease risk. Twelve single spore isolates collected from wheat-growing areas of the South Island of New Zealand representing the P. tritici-repentis population were characterised for the Ptr ToxA and ToxB genes, ToxA and ToxB, respectively, using two gene specific primers. The susceptibility of 10 wheat cultivars to P. tritici-repentis was determined in a glasshouse experiment by inoculating young plants with a mixed-isolate spore inoculum. All 12 New Zealand P. tritici-repentis isolates were positive for the ToxA gene but none were positive for the ToxB gene. Tan spot lesions developed on all inoculated 10 wheat cultivars, with cultivars ‘Empress’ and ‘Duchess’ being the least susceptible and ‘Discovery’, ‘Reliance’ and ‘Saracen’ the most susceptible cultivars to infection by the mixed-isolate spore inoculum used. The results indicated that the cultivars ‘Empress’ and ‘Duchess’ may possess a level of tolerance to P. tritici-repentis and would, therefore, be recommended for cultivation in regions with high tan spot incidence.


2006 ◽  
Vol 96 (8) ◽  
pp. 885-889 ◽  
Author(s):  
P. K. Singh ◽  
J. L. Gonzalez-Hernandez ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
...  

Race 3 of the fungus Pyrenophora tritici-repentis, causal agent of tan spot, induces differential symptoms in tetraploid and hexaploid wheat, causing necrosis and chlorosis, respectively. This study was conducted to examine the genetic control of resistance to necrosis induced by P. tritici-repentis race 3 and to map resistance genes identified in tetraploid wheat (Triticum turgidum). A mapping population of recombinant inbred lines (RILs) was developed from a cross between the resistant genotype T. tur-gidum no. 283 (PI 352519) and the susceptible durum cv. Coulter. Based on the reactions of the Langdon-T. dicoccoides (LDN[DIC]) disomic substitution lines, chromosomal location of the resistance genes was determined and further molecular mapping of the resistance genes for race 3 was conducted in 80 RILs of the cross T. turgidum no. 283/Coulter. Plants were inoculated at the two-leaf stage and disease reaction was assessed 8 days after inoculation based on lesion type. Disease reaction of the LDN(DIC) lines and molecular mapping on the T. turgidum no. 283/Coulter population indicated that the gene, designated tsn2, conditioning resistance to race 3 is located on the long arm of chromosome 3B. Genetic analysis of the F2 generation and of the F4:5 and F6:7 families indicated that a single recessive gene controlled resistance to necrosis induced by race 3 in the cross studied.


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.


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