Prevalence of ToxA-sensitive alleles of the wheat gene Tsn1 in Australian and Chinese wheat cultivars

2009 ◽  
Vol 60 (4) ◽  
pp. 348 ◽  
Author(s):  
Richard P. Oliver ◽  
Kasia Rybak ◽  
Peter S. Solomon ◽  
Margo Ferguson-Hunt
Keyword(s):  
Recent Survey ◽  
Stagonospora Nodorum ◽  
Wheat Cultivars ◽  
Pyrenophora Tritici Repentis ◽  
Wheat Gene ◽  
Chinese Wheat

A recent survey of worldwide isolates of Stagonospora nodorum showed that all Australian isolates expressed the host-specific toxin ToxA (Stukenbrock and McDonald 2007). In contrast, very few Chinese isolates did. All the Australian Pyrenophora tritici-repentis isolates that were tested expressed ToxA. We therefore postulated that the wheat gene that confers sensitivity to ToxA, Tsn1, would vary in prevalence in wheat cultivars in use in the two countries. Contrary to expectation, 10 out of 21 Chinese cultivars responded to ToxA as did 26 out of 46 Australian cultivars. The result suggests that ToxA has not had a determining effect on the survival of wheat cultivars in either country. They also suggest that despite the widespread use of Tsn1 markers in Australia, sensitive alleles are still commonplace. The removal of sensitive alleles from breeders’ lines could be readily achieved and could significantly affect the resistance of wheat to both diseases.

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.

Diversity of Puroindoline genes and their association with kernel hardness in Chinese wheat cultivars and landraces

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Xiaoyan Li ◽  
Yin Li ◽  
Mengya Zhang ◽  
Xiaofen Yu ◽  
Rui Hu ◽  
...  
Keyword(s):  
Kernel Hardness ◽  
Wheat Cultivars ◽  
Chinese Wheat

Distribution of the photoperiod insensitive Ppd-D1a allele in Chinese wheat cultivars

Euphytica ◽  
2008 ◽  
Vol 165 (3) ◽  
pp. 445-452 ◽  
Author(s):  
F. P. Yang ◽  
X. K. Zhang ◽  
X. C. Xia ◽  
D. A. Laurie ◽  
W. X. Yang ◽  
...  
Keyword(s):  
Wheat Cultivars ◽  
Chinese Wheat

Distribution, Frequency and Variation of Stripe Rust Resistance Loci Yr10, Lr34/Yr18 and Yr36 in Chinese Wheat Cultivars

2012 ◽  
Vol 39 (11) ◽  
pp. 587-592 ◽  
Author(s):  
Cuiling Yuan ◽  
Hui Jiang ◽  
Honggang Wang ◽  
Kun Li ◽  
Heng Tang ◽  
...  
Keyword(s):  
Stripe Rust ◽  
Rust Resistance ◽  
Stripe Rust Resistance ◽  
Wheat Cultivars ◽  
Chinese Wheat ◽  
Distribution Frequency

scholarly journals Stripe rust resistance and genes in Chinese wheat cultivars and breeding lines

Euphytica ◽  
2013 ◽  
Vol 196 (2) ◽  
pp. 271-284 ◽  
Author(s):  
Qing-Dong Zeng ◽  
De-Jun Han ◽  
Qi-Lin Wang ◽  
Feng-Ping Yuan ◽  
Jian-Hui Wu ◽  
...  
Keyword(s):  
Stripe Rust ◽  
Rust Resistance ◽  
Stripe Rust Resistance ◽  
Wheat Cultivars ◽  
Breeding Lines ◽  
Chinese Wheat

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.

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