Published online 27 March 2006
Published in Crop Sci 46:1212-1217 (2006)
© 2006 Crop Science Society of America
677 S. Segoe Rd., Madison, WI 53711 USA
CROP BREEDING & GENETICS
Identification and Monosomic Analysis of Tan Spot Resistance Genes in Synthetic Wheat Lines (Triticum turgidum L. x Aegilops tauschii Coss.)
Wuletaw Tadesse,
Sai L.K. Hsam,
Gerhard Wenzel and
Friedrich J. Zeller*
Technical University of Munich, Institute of Plant Breeding, Am Hochanger 2, D-85350 Freising- Weihenstephan, Germany
* Corresponding author (zeller{at}wzw.tum.de)
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ABSTRACT
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Tan spot, caused by the fungus Pyrenophora tritici-repentis (Died.) Drechs. (Ptr), anamorph Drechslera tritici-repentis (Died.) Shoem., is becoming a major yield limiting leaf disease of both durum (Triticum turgidum L. var durum) and common wheat (Triticum aestivum L.) worldwide. In this study, differential isolates and varieties were developed, and using the most virulent isolate, ASC1b, we screened about 100 synthetic wheat genotypes against the disease. Two (2%) and 20 (20.4%) of the genotypes were found to be immune and highly resistant, respectively. Monosomic analyses of the F2 hybrids (crosses of the highly resistant accessions (XX41, XX45) and the moderately resistant accession XX110 with the monosomic lines (D-genome) of the wheat cultivar Chinese Spring have revealed that the resistance genes are located on chromosome 3D. The gene in lines XX41 and XX110 showed a recessive monogenic inheritance, whereas the gene in line XX45 exhibited a dominant mode of inheritance. The recessive genes from XX41 and XX110 are tentatively named tsn3 and tsn-syn1, respectively, and the dominant gene from XX45 is named as Tsn-syn2.
Abbreviations: CIMMYT, International Wheat and Maize Improvement Center • CS, Chinese Spring • PDA, Potato Dextrose Agar • Ptr, Pyrenophora tritici-repentis • S.E., Standard Error • TUM, Technical University of Munich
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INTRODUCTION
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TAN SPOT is one of the major destructive foliar diseases of wheat occurring worldwide (Hosford, 1982; Tekauz, 1976). The pathogen can attack both durum and common wheat as well as numerous other grass species (Hosford and Bush, 1974; Ali and Francl, 2003). The incidence of tan spot and its economic importance has dramatically increasing since the 1970s all over the world (Hosford, 1982; Wiese, 1987). A yield loss of 3 to 50% in susceptible wheat varieties was reported in Canada and USA (Hosford, 1982; Riede et al., 1996). According to a recent report (Tekauz et al., 2004), tan spot was the most prevalent wheat leaf disease during the year 2003 in Canada. In Germany, reduction of grain yield due to this disease could range from 10 to 36% (Wolf and Hoffmann, 1993). Perello et al. (2003) have indicated the fast spreading and destructive nature of this disease in the southern Cone region of South America, including Argentina, Brazil, Chile, Paraguay, and Uruguay. Duveiller et al. (2005) reported an average reduction in yield of 30% in south Asia.
The fast spread of the pathogen Pyrenophora tritici-repentis is attributed to its stubble-borne nature, a shift toward soil conservation practices such as minimum and zero tillage, the trend away from stubble burning (Rees, 1982; Wolf and Hoffmann, 1993), and intensive wheat after wheat cultivation. These practices retain crop residues on the soil surface, resulting in an increase of inoculum, since the pathogen survives from one season to the next on wheat and grass stubble. Many of the semidwarf wheat cultivars introduced in Australia after 1960 have a high susceptibility to the disease (Rees et al., 1988), indicating that changes in genotypes and the narrow genetic base of the cultivated wheat lines may also play a role in the increased incidence of tan spot (Lamari et al., 2005).
Effective control of tan spot can be achieved with foliar fungicides such as propiconazole {cis-trans-1-[2-(2, 4-dichlorophenyl)-4-propyl-1,3-dioxolan-2-ylmethyl]-1H-1,2,4-triazole} and tebuconazole [(RS)-1-p-chlorophenyl-4,4-dimethyl-3-(1H-1,2,4-triazol-1-ylmethyl)pentan-3-ol] (Watkins et al., 1982), but costs may be prohibitive in addition to the negative ecological impact. The use of resistant cultivars, on the other hand, is believed to be cost effective, socially feasible, and ecologically safe. Research results to date indicate that there are possibilities of identifying resistance genes by screening wide arrays of wheat germplasm (Rees et al., 1988; Lamari and Bernier, 1989a; Mielke and Reichelt, 1999). Siedler et al. (1994) and more recently Xu et al. (2004) have reported the presence of resistance in synthetic wheat genotypes, which are hybrids between tetraploid wheats (T. turgidum) and diploid wild wheat (Aegilops tauschii Coss.).
There are different reports regarding the inheritance of tan spot resistance in wheat. Some researchers (Nagle et al., 1982; Elias et al., 1989; Faris et al., 1997; Effertz et al., 2002) reported quantitative inheritance, while others (Lamari and Bernier, 1989b, 1991; Gamba and Lamari, 1998; Lee and Gough, 1984) have reported the inheritance of tan spot is qualitative, controlled by single major recessive genes. More recently, Lamari et al. (2003) have also found that the inheritance of tan spot is qualitative indicating that a gene-for-gene relationship exists in the Triticum–P. tritici repentis system. However, to date only very few sources of resistance against the disease have been identified and mapped (Faris et al., 1996, 1997; Friesen and Faris, 2004; Cheong et al., 2004). Therefore, it is essential to undertake a constant search for novel resistance genes to cope with the dynamic and rapidly evolving pathogen population. Hence, this study was performed with the objectives of screening available synthetic wheat genotypes to identify further sources of resistance and to determine the chromosomal location of the genes.
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MATERIALS AND METHODS
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Plant Materials
Wheat cultivars (2n = 6x = 42, AABBDD)—Salamouni, Glenlea, Katepwa, Red Chief, 6B365, Chinese Spring, and Kanzler—were used for selection of differential isolates. A total of 98 synthetic wheat genotypes (2n = 6x = 42, AABBDD), which are amphiploids developed from the hybrid between tetraploid wheat (T. turgidum, 2n = 4x = 28, AABB) and Ae. tauschii (2n = 2x = 14, DD), were used for this study. Some of these lines were obtained from International Maize and Wheat Improvement Center (CIMMYT) and others were developed by the Division of Applied Genetics and Plant Breeding of the Technical University of Munich, Germany. Average of 10 seeds per genotype were planted in a pot (10-cm diameter) containing peat moss, at a temperature of approximately 20 to 23°C with 16 h of photoperiod in the greenhouse. Each genotype was replicated three times. Water was supplied by capillary action via holes in the base of the pots. Table 1 indicates the list and pedigrees of the synthetic wheat genotypes.
Inoculum Production
Three isolates, ASC1a, ASC1b, and 86–1241a, were kindly provided by Dr Lamari, University of Manitoba. Isolate Cz1–2 was obtained from Czech Republic. DTR 1/2000 and DTR 12/2000 were supplied from the Bavarian State Research Center for Agriculture (LFL), Germany, while the remaining two isolates, NunBr-1 and Rog5/04, were developed during the course of this study following the method described by Lamari and Bernier (1989a) from infected leaf samples collected in Nürnberg and Roggenstein areas of southern Germany, respectively. The isolates were screened for their effectiveness using standard varieties and cultivar Chinese Spring, and the most virulent isolate ASC1b (race 1) was selected and used both for the screening of synthetic genotypes and monosomic analysis.
Inoculum production followed the method of Lamari and Bernier (1989a) and Raymond et al. (1985). A single medium consisting of 150 mL V8 juice (Campbell Soup Company, Camden, NJ), 10 g Potato Dextrose Agar (PDA), 3 g CaCO3, 10 g Bacto agar (Difco, Detroit, MI), and 850 mL distilled water was prepared and poured into Petri dishes. Small plugs with 0.5-cm diameter from a 7-d-old culture of P. tritici-repentis were transferred singly into the above mentioned plates. The cultures were then incubated in the dark for about 8 d, flooded with sterile distilled water, and the mycelia were flattened with a sterilized glass rod. Water was decanted from the plates and the cultures were transferred to a regime of 24 h of light at room temperature followed by 22 h of darkness at 15°C. The light period enables for the formation of conidiophores while the dark period induces the formation of conidia. After 22 h of darkness, conidia were harvested by flooding the plates in sterile distilled water and scraping the spores from the plates. The concentration was adjusted approximately to 3000 spores mL–1.
Conidial Inoculation and Rating
Eight Ptr isolates—ASC1a, ASC1b, 86–124a, Nubr-1, Rog5/04, DTR 1–2000, and DTR 12–2000—were used for the development of differential varieties, while only the most virulent isolate (ASC1b) was used for the screening of synthetic lines and monosomic analysis. Plants were inoculated at the two leaf stage and were placed into a 2- x 1.5- x 1-m portable plastic tent inside the greenhouse. The tent was further covered by a black plastic sheet to ensure complete darkness. A relative humidity of 100% was maintained with a humidifier. After 24 h of leaf-wetness period in the dark as indicated above, the plants were transferred into a growth chamber at a temperature of 22°C and photoperiod of 12 h/day for about 7 d. The plants were evaluated for their resistance to tan spot 7 d after inoculation following the 0-to-5 rating scale with a little modification of the 0-to-5 rating scale developed by Lamari and Bernier (1989a): where 0 = immune, 1 = resistant, 2 = moderately resistant, 3 = moderately resistant to moderately susceptible, 4 = susceptible, 5 = highly susceptible.
Monosomic Analyses
Seven monosomic lines of the D genome of wheat cultivar Chinese Spring (CS), which is susceptible to tan spot, were crossed with three synthetic lines XX41, XX45, and XX110. CS monosomic lines and the three synthetic lines (2n = 6x = 42, AABBDD) were used as female and pollen parents, respectively. The synthetic lines XX41, XX45, and XX110 were previously tested in our laboratory and found to be highly resistant to mixtures of Ptr isolates (Siedler, 1991), and hence we used them further for monosomic crossing before screening of the 98 synthetic lines. The seven monosomic lines of Chinese Spring and the F1 crosses were screened for monosomy (2n = 41) by chromosome counts from squashes of root-tip cells pretreated with mono-bromonapthalene and stained by the Feulgen method (Zeller et al., 2002). Only confirmed 2n = 41 chromosome seedlings of the monosomic series of Chinese Spring and the F1 hybrids were planted (three seedlings per pot) in 50-cm diameter pot and raised in the greenhouse following standard wheat agronomic practices. Crosses of disomic cultivar Chinese Spring with XX41, XX45, and XX110 were made as controls to study the segregation and inheritance of tan spot resistance. The monosomic families were screened in three sets of inoculations using Ptr isolate ASC1b. For each set of inoculation, 17-d-old seedlings were raised by planting F2 seeds in three pots at a rate of 10 seeds per pot for each combination depending on the availability of seeds. Inoculum production, inoculation techniques and rating scales used for the screening of the synthetic lines were also applied here. Evaluation was made on single plant basis, and score values of 0, 1, and 2 were grouped as resistant while 3, 4, and 5 were grouped as susceptible. The number of resistant and susceptible plants in each set of inoculation was summed up to get the total frequency of susceptible and resistant F2 plants per each combination. 
2 analyses were performed using Agrobase 20 software (Agronomix Software Inc., 1990) to determine the goodness of fit either for a 3: 1 or 1:3 (resistant: susceptible) segregation.
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RESULTS AND DISCUSSION
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Differential Wheat Cultivars and Ptr Isolates
As indicated in Table 2, the cultivars responded differentially toward Ptr isolates possessing different virulence.
Salamouni, which was previously identified to be resistant, showed moderately susceptible response to isolates ASC1b, DTR1–2000, and DTR 12–2000. Glenlea, Katepwa, and Kanzler were susceptible to most of the isolates. The cultivar Red Chief showed resistant response across all the isolates. Cultivar Chinese Spring was susceptible to isolates ASC1a and ASC1b but moderately susceptible to the isolates Rog5/04, DTR1–2000, and DTR 12–2000.
Screening Synthetic Wheat Genotypes for Tan Spot Resistance
A total of 98 synthetic wheat lines were screened with the most virulent Ptr isolate ASC1b for their seedling resistance against tan spot caused by P.tritici-repentis. The response of the genotypes to Ptr ASC1b ranged from 0 (immune) to 5 (highly susceptible) with a mean value of 2.2 in the 0-to-5 scale (Table 1). Two genotypes (syn 38 and syn 44) were found to be immune and twenty genotypes were highly resistant. The majority of the genotypes (40.8%) were moderately resistant. Siedler (1991) had reported that lines XX41, XX45, and XX110 showed highly resistant response to mixtures of Ptr isolates. In the present study XX41 and XX45 were confirmed to be highly resistant, while XX110 was moderately resistant to the most virulent monoconidial Ptr isolate, ASC1b.
This result indicated the presence of broad level of resistance against tan spot from synthetic wheats. Similar results were reported previously by Siedler et al. (1994) and more recently by Xu et al. (2004).
Chromosomal Location
Three resistant synthetic genotypes, XX41 [a hybrid between Langdon durum and Ae. tauschii (CI 00017)], XX45 (Langdon durum/Ae. tauschii, RL 5565), and XX110 [(T. dicoccum Schrank (A38)/Ae. tauschii, CI 33] were crossed as pollen parents to the D genome Chinese Spring monosomic lines (1D-7D). The F1 hybrids were checked for monosomy and planted in the greenhouse to obtain F2 seeds. The results of the F2 monosomic analyses are indicated in Tables 3, 4, and 5.
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Table 3. Frequencies of resistant and susceptible seedlings in crosses of Chinese Spring monosomics and XX41 tested with Ptr isolate ASC1b.
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Table 4. Frequencies of resistant and susceptible seedlings in crosses of Chinese Spring monosomics and XX45 tested with Ptr isolate ASC1b.
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As expected, the F2 populations from the crosses between disomic Chinese Spring and the resistant parents XX41 and XX110 (Tables 3 and 5), segregated into 34 and 110 susceptible and 11 and 42 resistant plants, respectively, fitting a 1:3 (resistant: susceptible) Mendelian ratio, which indicated that the resistance in these two lines to tan spot was controlled by a single recessive gene. On the other hand, the F2 populations from crosses between disomic Chinese Spring and XX45 segregated into 97 resistant and 41 susceptible plants (Table 4), indicating that the resistance gene is dominant. This qualitative inheritance of the resistance genes is in agreement with previous reports of Lee and Gough (1984), Lamari and Bernier (1989b, 1991), Gamba and Lamari (1998), Lamari et al. (2003), and Singh and Hughes (2005). Parental lines of XX41 (Langdon durum and Aegilops tauchii, CI 00017), XX45 (Langdon durum and Aegilops tauschii, RL 5565), and XX110 (T. dicoccum, A38 and Aegilops tauschii, CI 33) were evaluated using Ptr isolate ASC 1b so as to identify the source of resistance in the respective synthetic lines. The tetraploid parents Langdon durum and T. dicoccum (A38) were susceptible (4 in 0-to-5 scale), while the diploid Ae. tauchii parents (CI 00017 and RL 5565) were highly resistant (1) and CI 33 was moderately resistant (2), indicating that the source of resistance in the synthetic lines was from the diploid Ae. tauschii lines.
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Table 5. Frequencies of resistant and susceptible seedlings in crosses of Chinese Spring monosomics and XX110 tested with Ptr isolate ASC1b.
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The 2 analyses of the segregation ratio from the three populations indicated that the combinations of mono-3D segregated differently and significantly (p < 0.01) from the expected 1:3 and 3:1 (resistant: susceptible) ratios indicating that these were the critical crosses. The segregation pattern in the critical crosses were 60: 5, 74: 4 and 70:7 resistant: susceptible plants in CS/XX41, CS/XX45 and CS/XX110 F2 populations, respectively. The results clearly indicated that the resistance genes are located on chromosome 3D. The recessive genes from XX41 and XX110 are tentatively designated tsn3 and tsn-syn1, respectively, and the dominant gene from XX45 is named Tsn-syn2. However, further studies of allelism tests and analyses of molecular markers are necessary to confirm whether the genes are allelic or at different loci. Resistance genes for tan spot have not been located on D-genome chromosomes in hexaploid wheat (Xu et al., 2004). Most of the tan spot resistant genes reported to date were located on the B-genome of hexaploid wheat. Faris et al. (1996) mapped the resistance locus tsn-1 on the long arm of 5B using restriction fragment length polymorphism (RFLP) markers. Friesen and Faris (2004) identified a QTL on the short arm of chromosome 2B and designated tsc2 using molecular analysis. A major QTL on 5BL, which actually is expected to be the same as tsn-1, was also reported from the Australian variety Brookton (Cheong et al., 2004). More recently, Faris and Friesen (2005) have identified QTL on chromosome arms 1BS and 3BL in cultivar BR34 using Ptr races 1–3 and 5 indicating presence of race- nonspecific tan spot resistance.
As compared with bread wheat, synthetic lines showed a large degree of genetic variation for resistance to different wheat diseases (Xu et al., 2004). In the present study, about 100 synthetic lines were screened for tan spot resistance. Two genotypes were found immune and 20 genotypes were highly resistant. Furthermore the chromosomal location of the resistance gene from the previously identified resistance lines (XX41, XX45, and XX110) was identified to be on chromosome 3D, which according to our knowledge, is the first report to locate tan spot resistance gene on D-genome of wheat. Allelism test of the immune/resistant lines such as syn 11, syn 38, syn 44, syn 84, syn 87, XX111, and XX195 with XX41, XX45, and XX110 to test the identity of the gene in one of these lines with the genes tsn-3, tsn-syn1, and Tsn-syn2 should be undertaken to confirm that they are different. The source of resistance in the synthetic lines XX41, XX45, and XX10 was identified to be the A. tauschii parent. Similarly, it is important to identify the source of resistance for the other synthetic lines. The immune and highly resistant lines identified in the present study including the lines used for the monosomic crosses (XX41, XX45, and XX110) are recommended to be used as parental lines for development of tan spot resistant wheat cultivars and mapping populations.
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ACKNOWLEDGMENTS
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The first author is supported by a scholarship from the German Academic Exchange Service (DAAD), Bonn.
Received for publication November 1, 2005.
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REFERENCES
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- Agronomix Software Inc. 1990. Agrobase 20. Winnipeg, Canada.
- Ali, S., and L.J. Francl. 2003. Population race structure of Pyrenophora tritici-repentis prevalent on wheat and none cereal grasses in the Great plains. Plant Dis. 87:418–422.[CrossRef]
- Cheong, J., H. Wallwork, and K.J. Williams. 2004. Identification of a major QTL for yellow leaf spot resistance in the wheat varieties Brookton and Cranbrook. Aust. J. Agric. Res. 55:315–319.
- Duveiller, E., Y.R. Kandel, R.C. Sharma, and S.M. Shrestha. 2005. Epidemiology of foliar blights (spot blotch and tan spot) of wheat in the plains bordering the Himalayas. Phytopathology 95:248–256.[Medline]
- Effertz, R.J., S.W. Meinhardt, J.A. Anderson, J.G. Jordal, and L.J. Francl. 2002. Identification of a chlorosis inducing toxin from Pyrenophora tritici-repentis and the chromosomal location of an insensitive locus in wheat. Phytopathology 92:527–533.[Medline]
- Elias, E., R.G. Cantrell, and R.M. Hosford, Jr. 1989. Heritability of resistance to tan spot in durum wheat and its associations with other agronomic traits. Crop Sci. 29:299–304.[Abstract/Free Full Text]
- Faris, J.D., J.A. Anderson, L.J. Francl, and J.G. Jordahl. 1996. Chromosomal location of a gene conditioning insensitivity in wheat to a necrotic inducing culture filtrate from Pyrenophora tritici-repentis. Phytopathology 86:459–463.[CrossRef][ISI]
- Faris, J.D., J.A. Anderson, L.J. Francl, and J.G. Jordahl. 1997. RFLP mapping of resistance to chlorosis induction by Pyrenophora tritici-repentis in wheat. Theor. Appl. Genet. 94:98–103.[CrossRef][ISI]
- Faris, J.D., and T.L. Friesen. 2005. Identification of quantitative trait loci for race-nonspecific resistance to tan spot in wheat. Theor. Appl. Genet. 111:386–392.[CrossRef][ISI][Medline]
- Friesen, T.L., and J.D. Faris. 2004. Molecular mapping of resistance to Pyrenophora tritici-repentis race 5 and sensitivity to Ptr ToxB in wheat. Theor. Appl. Genet. 109:464–471.[ISI][Medline]
- Gamba, F.M., and L. Lamari. 1998. Mendelian inheritance of tan spot (Pyrenophora tritici-repentis) in selected genotypes of durum wheat (Triticum durum). Can. J. Plant Pathol. 20:408–414.
- Hosford, R.M., Jr. 1982. Tan spot. p. 1–24. In R.M Hosford, Jr. (ed.) Tan spot of wheat and related diseases. North Dakota State University, Fargo.
- Hosford, R.M., Jr., and R.H. Bush. 1974. Losses in wheat caused by Pyrenophora trichostoma and Leptosphaeria avenaria f. sp. triticea. Phytopathology 64:184–187.
- Lamari, L., and C.C. Bernier. 1989a. Evaluation of wheat lines and cultivars to tan spot (Pyrenophora tritici-repentis) based on lesion type. Can. J. Plant Pathol. 11:49–56.
- Lamari, L., and C.C. Bernier. 1989b. Toxin of Pyrenophora tritici-repentis: Host specificity, significance in disease and inheritance of host reaction. Phytopathology 79:740–744.[CrossRef][ISI]
- Lamari, L., and C.C. Bernier. 1991. Genetics of tan necrosis and extensive chlorosis in tan spot of wheat caused by Pyrenophora tritici-repentis. Phytopathology 81:1092–1095.[CrossRef][ISI]
- Lamari, L., S.E. Strelkov, A. Yahyaoui, J. Orabi, and R.B. Smith. 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.[Medline]
- Lamari, L., B.D. McCallum, and R.M. dePauw. 2005. Forensic pathology of Canadian bread wheat: The case of tan spot. Phytopathology 95:144–152.[Medline]
- Lee, T.S., and F.J. Gough. 1984. Inheritance of Septoria leaf blotch (S. tritici) and Pyrenophora (P. tritici-repentis) resistance in Triticum aestivum cv. Carifen 12. Plant Dis. 68:848–851.
- Mielke, H., and A. Reichelt. 1999. Studien zur Biologie des Erregers Drechslera tritici-repentis zur Anfälligkeit des Weizens und verschiedener Artverwandter sowie zur Bekämpfung der DTR-Weizenblattdürre. Parey Verlag, Berlin.
- Nagle, B.J., R.C. Frohberg, and R.M. Hosford, Jr. 1982. Inheritance of resistance to tan spot of wheat. p. 40–45. In R.M Hosford, Jr. (ed.) Tan spot of wheat and related diseases. North Dakota State University, Fargo.
- Perello, A., V. Moreno, M.R. Simon, and M. Sisterna. 2003. Tan spot of wheat infection at different stages of crop development and inoculum type. Crop Prot. 22:157–169.[CrossRef]
- Raymond, P.J., W.W. Bockus, and B.L. Norman. 1985. Tan spot of winter wheat: Procedures to determine host response. Phytopathology 75:686–690.[ISI]
- Rees, R.G. 1982. Yellow spot, an important problem in the north eastern wheat areas of Australia. p. 68–70. In R.M Hosford, Jr. (ed.) Tan spot of wheat and related diseases. North Dakota State University, Fargo.
- Rees, R.G., G.J. Platz, and R.J. Mayer. 1988. Susceptibility of Australian wheats to Pyrenophora tritici-repentis. J. Agric. Res. 39:141–151.
- Riede, C.R., L.J. Francl, J.A. Anderson, J.G. Jordahl, and S.W. Meinhardt. 1996. Additional sources of resistance to tan spot of wheat. Crop Sci. 36:771–777.[Abstract/Free Full Text]
- Siedler, H. 1991. Untersuchungen zur Evaluierung von Resistanz gegenüber Pyrenophora tritici-repentis in Aegilops squarrosa und synthetischen Amphiploiden (Triticum turgidum ssp. x Aegilops squarrosa. MSc thesis, Technical University of Munich, Freising-Weihenstephan.
- Siedler, H., A. Obst, S.L.K. Hsam, and F.J. Zeller. 1994. Evaluation for resistance to Pyrenophora tritici-repentis in Aegilops tauchii Coss. and synthetic hexaploid wheat amphiploids. Genet. Res. Crop. Evol. 41:27–34.
- Singh, P.K., and G.R. Hughes. 2005. Genetic control of resistance to tan necrosis induced by Pyrenophora tritici-repentis, race 1 and race 2, in spring and winter wheat genotypes. Phytopathology 95:172–177.[Medline]
- Tekauz, A. 1976. Distribution, severity, and relative importance of leaf spot diseases of wheat in western Canada in 1974. Can. Plant Dis. Surv. 56:36–40.
- Tekauz, A., E. Mueller, M. Beyene, M. Stulzer, and D. Schultz. 2004. Leaf spot diseases of winter wheat in Manitoba in 2003. Can. Plant Dis. Surv. 83:73–74.
- Watkins, J.E., M.G. Boosalis, and B.L. Doupnik, Jr. 1982. Foliar diseases of Nebraska's winter wheat. p. 53–61. In R.M Hosford, Jr. (ed.) Tan spot of wheat and related diseases. North Dakota State University, Fargo.
- Wiese, M. 1987. Compendium of wheat diseases. American Phytopathology Society, St. Paul, MN.
- Wolf, P.F.J., and G.M. Hoffmann. 1993. Zur Biologie von Drechslera tritici-repentis (Died.) Shoem. (telomorph Pyrenophora tritici-repentis (Died.) Drechsler), dem Erreger einer Blattfleckenkrankheit an Weizen. Z. Pfl.krankh. Pflschutz 100:33–48.
- Xu, S.S., T.L. Friesen, and A. Mujeeb-Kazi. 2004. Seedling resistance to tan spot and Stagonospora nodorum blotch in synthetic hexaploid wheats. Crop Sci. 44:2238–2245.[Abstract/Free Full Text]
- Zeller, F.J., L. Kong, L. Hartl, V. Mohler, and S.L.K. Hsam. 2002. Chromosomal location of genes for resistance to powdery mildew in common wheat (Triticum aestivum L. em Thell.) 7. Gene Pm29 in line Pova. Euphytica 123:187–194.
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ABSTRACT
INTRODUCTION
