scholarly journals Lipid Profiles in Wheat Cultivars Resistant and Susceptible to Tan Spot and the Effect of Disease on the Profiles

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.

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.


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.


2005 ◽  
Vol 95 (2) ◽  
pp. 172-177 ◽  
Author(s):  
P. K. Singh ◽  
G. R. Hughes

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.


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.


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 68 ◽  
pp. 449-449
Author(s):  
S.K. Weith ◽  
H.J. Ridgway ◽  
I.C. Harvey ◽  
R.A. Craigie ◽  
E.E. Jones

Tan spot of wheat is caused by the fungus Pyrenophora triticirepentis (Ptr) with reported incidence in New Zealand increasing in recent years Lesions characteristic of Ptr infection being oval tan spots surrounded by a chlorotic halo were observed on wheat leaves in 15 different wheat paddocks throughout the South Island in the 201314 season Fungal isolates recovered from these lesions on potato dextrose agar produced greygreen fluffy mycelium characteristic of Ptr Speciesspecific PCR using published primers (PtrUniqueF2/ PtrUniqueR2) generated a PCR product of 490 bp diagnostic of Ptr Sequencing of the rDNA and 946;tubulin gene regions confirmed the identification Ptr was found to be widely distributed throughout the wheat growing areas in the South Island from Southland to North Canterbury A postharvest farmer questionnaire was also undertaken Questionnaire answers revealed that continuous sowing of untreated wheat seed conservative tillage and low rate applications of fungicides may have exacerbated the severity of tan spot outbreaks during the 201314 season Further work to identify susceptible wheat cultivars and sensitivity to fungicides is currently under way


Plant Disease ◽  
2002 ◽  
Vol 86 (9) ◽  
pp. 1050-1050 ◽  
Author(s):  
S. Ali ◽  
L. J. Francl

Pyrenophora tritici-repentis causes tan spot of wheat worldwide. Fungal isolates have been characterized into seven races based on their ability to induce necrosis and chlorosis on appropriate wheat differentials (1,2). Nineteen single-spore isolates of P. tritici-repentis were recovered from diseased wheat leaves collected from Brazil. The isolates were tested for their race structure by individually inoculating a suspension of 3,000 conidia per ml on wheat differential seedlings at the 2-leaf stage in the greenhouse. The isolates were tested three times and consistent results were found. The differential set was comprised of Glenlea, Katepwa, ND495, 6B365, Salamouni, and M-3. Seven of the 19 isolates were grouped into race 1 because they produced necrosis on Glenlea, Katepwa, and ND495; chlorosis on 6B365; and neither symptom on Salamouni and M-3. Twelve of the isolates produced necrosis on Glenlea, Katepwa, ND495, 6B365, and Salamouni, and neither symptom on M-3. Necrotic reactions to these isolates on 6B365 (chlorotic or resistant to currently identified 7 races) and Salamouni (resistant to all 7 races), and the resistant reaction on M-3 (resistant to all 7 races) differentiate them from the other seven races. Therefore, we grouped these isolates under a new race and designated this as race 8. To our knowledge, this is the first report on the occurrence of race 8 in P. tritici-repentis. This discovery holds particular significance to breeders and pathologists interested in producing wheat lines with resistance to tan spot. Additionally, we suggest that M-3 be added to the differential set because this line is resistant to all eight identified races. More isolates from Brazil are under investigation to discover the P. tritici-repentis race structure in the country. References: (1) S. Ali et al. (Abstr.) Phytopathology 92(suppl):S3, 2002. (2) S. E. Strelkov et al. Can. J. Plant Pathol. 24:29, 2002.


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