Evaluation of Wheat Lines and Cultivars to tan Spot [Pyrenophora Tritici-Repentis] Based on Lesion Type

1989 ◽  
Vol 11 (1) ◽  
pp. 49-56 ◽  
Author(s):  
L. Lamari ◽  
C.C. Bernier
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.


2007 ◽  
Vol 114 (5) ◽  
pp. 855-862 ◽  
Author(s):  
W. Tadesse ◽  
M. Schmolke ◽  
S. L. K. Hsam ◽  
V. Mohler ◽  
G. Wenzel ◽  
...  

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.


2003 ◽  
Vol 93 (4) ◽  
pp. 397-401 ◽  
Author(s):  
T. L. Friesen ◽  
S. Ali ◽  
S. Kianian ◽  
L. J. Francl ◽  
J. B. Rasmussen

Pyrenophora tritici-repentis race 2 produces Ptr ToxA, a host-selective toxin previously described as a pathogenicity factor for tan spot on wheat. The objective of this research was to evaluate the role of host sensitivity to toxin, conditioned by a single dominant gene on chromosome 5BL, in the disease development by race 2. An F2-derived F6 recombinant inbred population of 108 wheat lines, produced from crosses of toxin-sensitive, disease-susceptible cv. Kulm with the toxin-insensitive, disease-resistant cv. Erik segregated 1:1 for toxin reaction. However, the population was skewed toward resistance to race 2 of the fungus. Toxin reaction accounted for 24.4% of the genetic variance for disease. Heritability estimates suggested the presence of four to five genes that influence disease reaction in the population. Toxin-insensitive mutants, previously derived Kulm, were susceptible to race 2, although disease developed more slowly on the mutants than it did on the wild-type Kulm. The data indicate that sensitivity to Ptr ToxA influences disease severity in some host genotypes without defining susceptibility.


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.


2020 ◽  
Vol 110 (11) ◽  
pp. 1781-1790
Author(s):  
Jingwei Guo ◽  
Gongjun Shi ◽  
Audrey Kalil ◽  
Andrew Friskop ◽  
Elias Elias ◽  
...  

The ascomycete fungus Pyrenophora tritici-repentis is the causal agent of tan spot of wheat. The disease can occur on both common wheat (Triticum aestivum) and durum wheat (T. turgidum ssp. durum) and has potential to cause significant yield and quality losses. The fungal pathogen is known to produce necrotrophic effectors (NEs) that act as important virulence factors. Based on the NE production and virulence on a set of four differentials, P. tritici-repentis isolates have been classified into eight races. Race 4 produces no known NEs and is avirulent on the differentials. From a fungal collection in North Dakota, we identified several isolates that were classified as race 4. These isolates caused no or little disease on all common wheat lines including the differentials; however, they were virulent on some durum cultivars and tetraploid wheat accessions. Using two segregating tetraploid wheat populations and quantitative trait locus mapping, we identified several genomic regions significantly associated with disease caused by two of these isolates, some of which have not been previously reported. This is the first report that race 4 is virulent on tetraploid wheat, likely utilizing unidentified NEs. Our findings further highlight the insufficiency of the current race classification system for P. tritici-repentis.


1999 ◽  
Vol 89 (6) ◽  
pp. 444-449 ◽  
Author(s):  
Lynda M. Ciuffetti ◽  
Robert P. Tuori

Tan spot of wheat, caused by the fungus Pyrenophora tritici-repentis, is a destructive disease found in wheat-growing regions worldwide that can lead to serious yield losses. Changes in cultural practices have led to an increase in the severity and incidence of tan spot. Following infection, compatible races of the fungus elicit two distinct symptoms in differential wheat lines: tan necrosis and (extensive) chlorosis. Tan necrosis has been clearly demonstrated by several groups to result from the action of a protein toxin, Ptr ToxA. Wheat sensitivity to this toxin is conditioned by a single dominant gene. The chlorosis response may be more complex and appears to involve at least two other toxins, Ptr ToxB and Ptr ToxC, produced by different races of the fungus. Distinct genes apparently condition the reaction of wheat lines to each of these chlorosis-inducing toxins. This review concentrates on significant advances that have occurred during the past decade in the characterization of this disease interaction, ranging from the epidemiology and management of tan spot to molecular host-parasite interactions. Particular emphasis is placed on work describing fungal race differentiation, production of toxins and their importance in pathogenicity, and the genetics and physiology of host response to infection.


2017 ◽  
Vol 38 (SI 2 - 6th Conf EFPP 2002) ◽  
pp. 302-304 ◽  
Author(s):  
A. Shaukat ◽  
L.J. Francl

Knowledge of genetic variation in a pathogen population contributes to breeding for disease resistance. The fungus Pyrenophora tritici-repentis, cause of tan spot of wheat, is an important foliar pathogen worldwide. Currently, eight races have been identified in the fungal population prevalent on wheat and alternative hosts. Races 1 through 6 have been observed in North America. However, the fungal population from South America has not been characterized as to race. In this study, 48 single-spore isolates of P. tritici-repentis, recovered from wheat, were obtained from Argentina (10), Brazil (23), and Uruguay (15). Isolates were tested by inoculating individually on 2-leaf stage seedlings of the wheat differentials Glenlea, Katepwa, ND495, 6B365, M-3, and Salamouni in the greenhouse. They were grouped into different races based on necrosis and chlorosis induction on the differentials. Isolates from Argentina were grouped into races 1 and 7; from Brazil into races 1 and 8; and, from Uruguay into races 1 and 2. Results indicate that P. tritici-repentis has a diverse population on wheat in South America. More isolates are under investigation to obtain a comprehensive virulence pattern of the pathogen population in South America. Wheat lines should be screened against all known races to achieve durable resistance in a cultivar release program. The P. tritici-repentis race structure on wheat in Europe needs to be determined, as the pathogen has become a concern for wheat breeders and pathologists.


Plant Disease ◽  
1999 ◽  
Vol 83 (3) ◽  
pp. 269-273 ◽  
Author(s):  
C. K. Evans ◽  
R. M. Hunger ◽  
W. C. Siegerist

Incorporation of tan spot resistance into adapted wheat (Triticum aestivum) lines requires screening procedures in the greenhouse and field that correctly identify reaction to tan spot. This study compares greenhouse (seedling) and field (adult plants) testing of wheat lines for reaction to tan spot following inoculation with conidia by Pyrenophora tritici-repentis. Mistirrigation was used to provide adequate moisture for infection by P. tritici-repentis in the greenhouse and in the field. Reaction of seedlings to tan spot in the greenhouse was measured by lesion length. Area under the disease progress curve (AUDPC) was used to determine reaction in the field. The effect of tan spot on grain yield and kernel weight was determined by comparing inoculated with fungicide-sprayed split-plot values. In greenhouse tests, lesion length ranged from 1.2 to 4.1 mm. Lesions were 1.2 mm long on Red Chief, a tan spot-resistant check. Lesions were 3.6 mm long on TAM 105, a tan spot-susceptible check. Four breeder lines had levels of seedling (greenhouse) resistance nearly equal to that of Red Chief. Ranks of lesion length and field assessments of the AUDPC were significantly correlated (r = 0.75 to 0.93, P ≤0.05). Thus, greenhouse assessment was useful for screening large numbers of wheat genotypes for reaction to tan spot and identifying selected entries for further screening in the field. Mean grain yield from P. tritici-repentis inoculated plots was approximately 15% less than yield from fungicide-sprayed plots. Kernel weight was reduced an average of 7 and 13% at two field locations.


2005 ◽  
Vol 95 (2) ◽  
pp. 144-152 ◽  
Author(s):  
Lakhdar Lamari ◽  
Brent D. McCallum ◽  
Ron M. dePauw

Pyrenophora tritici-repentis causes necrosis and chlorosis in its wheat host. Susceptibility to races 2 (necrosis) and 5 (chlorosis) of the pathogen is known to be mediated by Ptr ToxA and Ptr ToxB, respectively. Sensitivity to each toxin is controlled by a single dominant and independently inherited gene. We used sensitivity to Ptr ToxA and Ptr ToxB as two genetic markers to investigate the origin and the state of tan spot susceptibility in Canadian Western Red Spring (CWRS) wheat over a period of more than a century. Sensitivity to Ptr ToxA, the toxin produced by nearly all isolates of the pathogen collected in the past 20 years in western Canada, appears to have been present in the first major cultivar, Red Fife, grown massively in the late 1800s. Sensitivity then was transmitted unknowingly into Canadian wheat lines through extensive use of backcrossing to maintain the Marquis-Thatcher breadmaking quality. Sensitivity to Ptr ToxA, which nearly disappeared from cultivars grown in western Canada in the 1950s, was reintroduced in the 1960s and unintentionally bred into many of the present-day cultivars. Sensitivity to Ptr ToxB, a toxin rarely found in isolates from western Canada, appeared with the release of Thatcher in 1934 and was transferred to many cultivars through backcross programs. In spite of large areas planted to Ptr ToxAand Ptr ToxB-sensitive cultivars over decades, tan spot epidemics remained sporadic until the 1970s. The results of this study raise the problem of the narrowing genetic base of CWRS wheat lines and the potential for unanticipated threats from plant pathogens. The intercrossing of genetically diverse material in one Canadian wheat breeding program resulted in the release of several modern cultivars with resistance to tan spot. The absence of wild-type Ptr ToxB-producing isolates in western Canada remains unexplained, given that sensitivity to Ptr ToxB was present continuously in western Canadian cultivars grown on vast areas for more than 70 years.


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