Adhikari TB

Ali S

Mergoum M

Singh PK

English

Sydney eScholarship

 1Genetic analysis of wheat-Pyrenophora tritici-repentis interactions  Singh PK1, Mergoum M1, Ali S2, Adhikari TB2 1Department of Plant Sciences, North Dakota State University, Fargo, ND, USA 58102. 2Department of Plant Pathology, North Dakota State University, Fargo, ND, USA 58102  ABSTRACT Tan spot of wheat, caused by the fungus Pyrenophora tritici-repentis, is a destructive disease worldwide that can cause serious losses in quality and quantity of wheat grain production. The fungus induces two distinct symptoms; tan necrosis and extensive chlorosis, on susceptible wheat cultivars. The major objective of this study was to determine the genetic control of resistance to tan spot, caused by multiple races of P. tritici-repentis in the newly identified sources of resistance. Plants were inoculated at the two-leaf stage under controlled environmental conditions and disease assessment was based on lesion-type rating scale. The segregating generations of each cross were analysed for the allelism and/or inheritance studies. A single recessive gene controlled resistance to tan necrosis caused by race 1 in both tetraploid and hexaploid resistant genotypes studied. The lack of segregation in the inter- and intra-specific crosses between the resistant tetraploid and hexaploid genotypes indicates that they possess the same genes for resistance to tan necrosis and extensive chlorosis induced by P. tritici-repentis race 1. Two independent genes, a single dominant gene for extensive chlorosis in hexaploid wheat and a single recessive gene for tan necrosis in tetraploid wheat, controlled resistance to tan spot induced by race 5. Genetic analysis of inter- and intra-specific crosses among Triticum species confirms that wheat-P. tritici-repentis host-pathosystem follows the toxin model of gene-for gene hypothesis. INTRODUCTION Tan spot, a foliar disease of wheat, is caused by the fungus Pyrenophora tritici-repentis (Died.) Drechs (PTR). The tan spot disease syndromes induced on susceptible durum and common wheat consist of two phenotypically distinct and independent symptoms: tan necrosis and extensive chlorosis. On an average, tan spot causes 5 to 15% yield losses; however, under conditions favourable for disease development, it can cause up to 50% yield loss (1). Tan spot also adversely affects the quality of grain by causing grain shrivelling, dark smudge and black point (1). Currently, eight races of PTR have been identified based on their ability to induce necrosis and/or chlorosis on a set of differential wheat cultivars (6). Resistance is expressed as small, dark brown lesions that do not increase in size, while susceptibility is expressed as dark brown spots surrounded by tan necrosis and/or extensive chlorosis that may involve the entire leaf.  To date, three host-specific toxins (e.g., Ptr ToxA, Ptr ToxB, and Ptr ToxC) produced by the tan spot fungus have been identified and well-characterized. Genetic studies have established that the same gene controls sensitivity to the toxins and susceptibility to their producer races (2,4).  Information coming out of genetic studies reveals which germplasm and breeding strategy is to be adopted to develop cultivars containing the desired traits. Several independent studies on tan spot host-pathogen interactions revealed that resistance is inherited qualitatively (2,4,8) or quantitatively (2,7). Singh et al. (9) screened 975 accessions of wheat and its related species and identified new sources of resistance effective against PTR races 1, 2, 3, and 5. The objectives of this study were to i) determine the genetic control of resistance to PTR races 1 and 5 in the newly identified sources of resistance coming from different Triticum species, and ii) determine through allelic/genic studies the relationship between resistance genes. MATERIALS AND METHODS Genetic material and population development. Eight cultivars, selected for this study based on their reaction to PTR races 1 and 5 (9), were used to produce 10 cross populations. Each F1 plant grown to produce F2 seed was harvested separately and the F2 populations derived from each F1 plant were tested individually for disease reaction. Similarly, all F2:3 and F2:5 families were produced by single seed descent.   Disease screening. The isolates Ptr D-2000-HT VI-5 (PTR race 1) and Ptr DW-13 (PTR race 5) were used to produce spore inoculum for disease induction. The conidial inoculum production, disease screening, and its assessment were done following the procedures described by Lamari and Bernier (4). The seedlings were rated for disease reaction based on the 1 to 5 lesion-type rating scale, with plants having ratings of 1 and 2 considered resistant and those with ratings of 3 to 5 classified as susceptible. Statistical analysis.  The chi-square test for goodness-of-fit to various genetic models was applied to the segregation data observed for the F2 plants and the F2:3 or F2:5 families to determine the number of genes controlling resistance to tan spot of wheat. RESULTS Genetics of resistance to PTR race 1 Inheritance studies. All resistant/susceptible (R/S) crosses studied were observed to segregate for the necrosis component of tan spot caused by race 1 and segregation did not occur for the chlorosis component. All the F1 plants of the R/S crosses were susceptible, indicating that resistance to necrosis was recessive  2 (Table 1). The F2 generation of the R/S crosses segregated in a 1 resistant: 3 susceptible ratio, indicating that a single gene controlled resistance and confirming that resistance to necrosis was recessive in all crosses studied (Table 1). The F2:3 families of all R/S crosses segregated in the ratio 1 homozygous resistant: 2 segregating: 1 homozygous susceptible, thus confirming the hypothesis of monogenic control of resistance to necrosis caused by race 1 (Table 2).  Allelism studies. All the resistant parents involved in development of the crosses studied with race 1, were resistant to chlorosis. In each of the crosses, which were resistant/resistant (R/R) crosses for segregation to chlorosis by race 1, all F1 and F2 plants tested were resistant (Table 1). Confirmation of the lack of segregation of single-plant data was done by screening F2:3 families of all the crosses. The lack of segregation for chlorosis confirms that the resistant sources from both tetraploid and hexaploid wheat shared the resistance gene(s) controlling chlorosis induced by race 1 (Table 2). All F1 plants of the R/R crosses of resistant hexaploid genotypes with the resistant hexaploid check cultivar Erik were resistant to necrosis induced by race 1 (Table 1). However, while most F2 plants of these crosses were resistant, a few plants in four of the five crosses gave a moderately susceptible necrotic reaction (rating 3). None of the segregations of the R/R crosses fit a ratio, indicating that the resistant sources possessed different resistance genes. All the F2:3 families of each of the crosses tested were homozygous resistant, thus confirming that all the six resistant parents shared the same resistance gene (Table 2). All F1 and F2 generations and F2:3 families of the cross between resistant tetraploid genotype T. turgidum # 283 (TT# 283) and resistant hexaploid cultivar Erik did not segregate for resistance (Tables 1,2). These results confirm that the tetraploid and hexaploid resistant genotypes shared the same single gene for resistance to necrosis induced by race 1.  Genetics of resistance to PTR race 5 Inheritance studies. All F1 plants of the R/S crosses among the hexaploid wheat genotypes were resistant, indicating that resistance to chlorosis caused by race 5 was dominant (Table 1). The F2 generations of the R/S intra-specific crosses segregated in a 3 resistant: 1 susceptible ratio, indicating that a single gene controls resistance and confirming that resistance to chlorosis was dominant in all the crosses studied. The F2:5 families of all four R/S crosses segregated in the ratio 7 homozygous resistant: 2 segregating: 7 homozygous susceptible, thus confirming the hypothesis of monogenic control of resistance to chlorosis induced by race 5 in hexaploid wheat (Table 2). In the tetraploid cross T. turgidum # 283/Coulter, which was segregating for necrosis component of tan spot, the F1 and F2 generations and F2:5 families indicated that a single recessive gene control (Tables 1,2). Allelism studies. All F1 and F2 generations of the R/R crosses involving hexaploid wheat genotypes when tested with race 5 showed a resistant reaction (Table 1). Individual plant data were confirmed by screening F2:3 families of each of the R/R crosses which gave resistant reaction confirming that all resistant sources possessed the same gene for resistance to chlorosis induced by race 5 (Table 2). All the F1 and F2 plants and F2:3 families of the inter-specific cross between the resistant tetraploid and the resistant hexaploid source showed a resistant reaction confirming that resistance to race 5 in both tetraploid and hexaploid wheat were controlled by the same gene (Tables 1,2). The genetic studies with race 5 between susceptible genotypes Coulter (tetraploid) and Katepwa (hexaploid) gave interesting results. Coulter is susceptible to necrosis while Katepwa is susceptible to chlorosis caused by race 5. All F1 plants of the cross Coulter/Katepwa were susceptible. Plants of the F2 generation of this cross segregated for both necrosis and chlorosis. Rating plants for both necrosis and chlorosis components separately are error prone and hence disease scoring for resistant and susceptible (necrosis and/or chlorosis) reaction was performed. The F2 generation of this inter-specific S/S cross segregated in a 3 resistant: 13 susceptible ratio, indicating that different genes control susceptibility to race 5 in this cross (Table 1). The F2:3 families of this cross segregated for 1 homozygous resistant: 15 susceptible (homozygous and heterozygous families), confirming that different genes control susceptibility to necrosis (tetraploid) and chlorosis (hexaploid) in this cross (Table 2). DISCUSSION The resistant parents analysed in this study were genetically diverse but the allelic studies for resistance to PTR races 1 and 5 indicate that all the resistant sources possess the same gene(s) for resistance to tan spot. These findings agree with earlier studies (3,5,8) wherein different sources of resistance had no allelic differences. The allelic findings suggest that the wheat gene pool possesses very narrow genetic diversity for resistance to tan spot and hence rigorous efforts should continue to seek new and different genes for resistance.  Lamari et al. (6) suggested that the wheat-PTR interaction conforms to the toxin model of gene-for-gene hypothesis. The susceptibility interaction occurs due to the production of a toxin by the pathogen and the presence of a ‘toxin-receptor’ site in the host. If the presence of such a site is considered, the product of a susceptibility gene, then the resistance in the wheat-PTR pathosystem is due to lack of a susceptibility gene(s) rather than the presence of a resistance gene(s). This could be the reason why most studies have identified the same resistance gene(s) using the known races of PTR.   ACKNOWLEDGEMENTS Financial support from Saskatchewan Agriculture Development Fund, SK, Canada and State Board of Agricultural Research and Education, ND, USA is gratefully acknowledged.   3TABLE 1. Reaction of F1 and F2 seedlings of wheat crosses to Pyrenophora tritici-repentis race 1 and 5 evaluated in greenhouse. *Probability of obtaining deviations from the expected ratio is by chance alone and the observed population does not differ significantly from expected hypothesis. TABLE 2. Reaction of F2:3 and F2:5 families of wheat crosses to Pyrenophora tritici-repentis race 1 and 5 evaluated in greenhouse.   Cross F2:3 and F2:5 families R       Seg      S Ratio tested χ2 value Inheritance studies with race 1 2000 Spelt # 20/Kenyon 15 45 20 1:2:1 1.87* CIMMYT # 18/Kenyon 14 44 22 1:2:1 1.50* Altar Synthetic/Kenyon 13 42 25 1:2:1 3.13* TT  # 283/Coulter 17 33 20 1:2:1 0.36* Allelism studies with race 1 2000 Spelt # 20/Erik 80 0 0 1:0:0 -Intros Line # 7/Erik 80 0 0 1:0:0 - Altar Synthetic/Erik 80 0 0 1:0:0 - TT  # 283/Erik 70 0 0 1:0:0 - Inheritance studies with race 5 2000 Spelt # 20/Kenyon 33 14 33 7:2:7 1.83* CIMMYT # 18/Kenyon 38 14 28 7:2:7 3.28* Altar Synthetic/Kenyon 34 16 30 7:2:7 4.34* TT # 283/Coulter 32 11 37 7:2:7 0.47* Allelism studies with race 5 2000 Spelt # 20/Erik 80 0 0 1:0:0 - CIMMYT # 18/Erik 80 0 0 1:0:0 - Altar Synthetic/Erik 80: 0 0 1:0:0 - TT # 283/Erik 70 0 0 1:0:0 - Coulter/Katepwa 4 ---66-- 1:15 0.85* *Probability of obtaining deviations from the expected ratio is by chance alone and the observed population does not differ significantly from expected hypothesis.  REFERENCES 1. De Wolf, E. D., Effertz, R. J., Ali, S., and Francl, L. J. 1998. Vistas of tan spot research. Can. J. Plant Pathol. 20:349-370. 2. Elias, E., Cantrell, R. G., and Horsford, R. M., Jr. 1989. Heritability of resistance to tan spot in durum wheat and its association with other agronomic traits. Crop Sci. 29:299-304.  3. Gamba, F. M., Lamari, L., and Brûlé-Babel, A. 1998. Inheritance of race-specific necrotic and chlorotic reactions induced by Pyrenophora tritici-repentis in hexaploid wheats. Can. J. Plant Pathol. 20:401-407. 4. Lamari, L., and Bernier, C. C. 1989. Evaluation of wheat lines and cultivars to tan spot (Pyrenophora tritici-repentis) based on lesion type. Can. J. Plant Pathol. 11:49-56. 5. Lamari, L., and Bernier, C. C. 1989. Toxin of Pyrenophora tritici-repentis: host specificity, significance in disease, and inheritance of host reaction. Phytopathology 79:740-744.   6. Lamari, L., Strelkov, S. E., Yahyaoui, A., Orabi, J., and Smith, R. B. 2003. The identification of two new races of Pyrenophora tritici-repentis from the host center of diversity confirms a one-to-one relationship in tan spot of wheat. Phytopathology 93:391-396. 7. Nagle, B. J., Frohberg, R. C., and Hosford, R. M. Jr. 1982. Inheritance of resistance to tan spot of wheat. Pages 40-45 in: Tan Spot of Wheat and Related Diseases Workshop. R. M. Hosford Jr., ed. North Dakota State University, Fargo, N.D. 8. Singh, P. K., and Hughes, G. R.  2005. Genetic control of resistance to tan necrosis induced by Pyrenophora tritici-repentis, races 1 and 2, in spring and winter wheat genotypes. Phytopathology 95:172-177. 9. Singh, P. K., Mergoum, M., Ali, S., Adhikari, T. B., Elias, E. M., and Hughes, G. R. 2006. Identification of new sources of resistance to tan spot, Stagonospora nodorum blotch, and Septoria tritici blotch of wheat. Crop Sci. 46: 2047-2053.    Cross F1      R    S F2  R       S Ratio tested χ2 value Inheritance studies with race 1 2000 Spelt # 20/Kenyon 0 7 74 177 1:3 2.69* CIMMYT # 18/Kenyon 0 9 61 198 1:3 0.29* Altar Synthetic/Kenyon 0 8 54 202 1:3 2.08* TT # 283/Coulter 0 7 74 181 1:3 2.19* Allelism studies with race 1 2000 Spelt # 20/Erik 8 0 178 2 1:0 - CIMMYT # 18/Erik 8 0 248 8 1:0 - Altar Synthetic/Erik 9 0 255 1 1:0 - TT # 283/Erik 7 0 192 0 1:0 - Inheritance studies with race 5 2000 Spelt # 20/Kenyon 7 0 149 59 3:1 1.26* CIMMYT # 18/Kenyon 8 0 150 58 3:1 0.92*Altar Synthetic/Kenyon 7 0 157 63 3:1 1.55* TT # 283/Coulter 0 8 45 172 1:3 2.10* Allelism studies with race 5 2000 Spelt # 20/Erik 7 0 220 0 1:0 - CIMMYT # 18/Erik 9 0 201 0 1:0 - Altar Synthetic/Erik 8 0 212 0 1:0 - TT # 283/Erik 9 0 221 0 1:0 - Coulter/Katepwa 0 9 13 63 3:13 0.13* 

Genetic analysis of wheat Pyrenophora tritici-repentis interactions

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Genetic analysis of wheat Pyrenophora tritici-repentis interactions

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