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Published in Crop Sci. 44:2043-2048 (2004).
© 2004 Crop Science Society of America
677 S. Segoe Rd., Madison, WI 53711 USA

CROP BREEDING, GENETICS & CYTOLOGY

Genetics of Resistance to Stagonospora Nodorum Blotch of Hexaploid Wheat

Jie Fenga, Hong Mab and Geoff R. Hughesa,*

a Dep. of Plant Sciences, Univ. of Saskatchewan, 51 Campus Drive, Saskatoon, SK, S7N 5A8, Canada
b Pacific Northwest Research Institute, Seattle, WA 98122

* Corresponding author (geoff.hughes{at}usask.ca)


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The genetic control of resistance to Stagonospora nodorum blotch (SNB), caused by Stagonospora nodorum (Berk.) E. Castell. and E.G. Germano, an important foliar and head disease of wheat (Triticum aestivum L.) in many parts of the world, was investigated in five hexaploid winter wheat and one hexaploid spring wheat genotypes. F1 plant reaction and segregation data for resistance to a single Saskatchewan isolate of S. nodorum from various combinations of F2, random inbred line and doubled haploid (DH) populations of each resistant x susceptible cross indicated that single recessive genes controlled resistance in winter wheat genotypes ‘Red Chief’, ‘Hadden’, ‘Missouri Queen’, ‘Coker 76-35’ and 81IWWMN 2095, and in spring wheat line 86ISMN 2137. All disease tests were performed on plants at the three-leaf stage under controlled environmental conditions. Tests of F1, F2, F2:3, and DH populations from resistant x resistant crosses indicated that these six genotypes carried the same gene. The chromosomal location of this gene was determined by cytogenetic analysis with ‘Chinese Spring’ monosomic and ditelosomic lines. Tests of F1 and F2 plants from crosses between Red Chief and Chinese Spring monosomic and ditelosomic lines indicated that the gene shared by these hexaploid wheat genotypes is located on the long arm of chromosome 3A.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
STAGONOSPORA NODORUM BLOTCH caused by the necrotrophic fungus Stagonospora nodorum (Berk.) E. Castell. and E.G. Germano [syn. Septoria nodorum (Berk.) Berk. in Berk. and Broome] [teleomorph: Phaeosphaeria nodorum (E. Müll.) Hedjar. (syn. Leptosphaeria nodorum E. Müll.)] is an important foliar and head disease of wheat in most wheat-producing areas in the world. In Saskatchewan, SNB is one of the most common and important diseases on wheat and has been estimated to cause a 15% yield loss annually (DePauw, 1995).

Cultural practices, fungicide application, and resistant cultivars have been used to control SNB, but growing resistant cultivars is the most economic and effective strategy. Most genetic studies have indicated that host resistance to SNB is under polygenic control (Nelson and Gates, 1982; Ecker et al., 1989; Wilkinson et al., 1990; Bostwick et al., 1993; Wicki et al., 1999) thus, making it difficult to select for and to utilize resistance in breeding programs. However, several single genes controlling a high level of resistance in the seedling stage in wheat and wheat relatives have been reported (Frecha, 1973; Ma and Hughes, 1995; Murphy et al., 2000).

A recessive gene controlling resistance to SNB in a durum (T. durum Desf.) line was identified and named temporarily as SnbTM (Ma and Hughes, 1995). Since the methods used in the study by Ma and Hughes (1995) were successful in identifying major genes in resistant cultivars and segregating populations, this study used similar disease test protocols to determine (i) the genetic control of resistance to SNB in selected resistant hexaploid wheats, (ii) the allelic relationship of the resistance genes in hexaploid wheat, and (iii) the chromosomal location of the gene(s) identified.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Population Development
The plant materials used were (i) five resistant hexaploid winter wheat genotypes, including cultivars Coker 76-35, Hadden, Missouri Queen, Red Chief and line 81IWWMN 2095, and resistant hexaploid spring wheat line 86ISMN 2137; (ii) susceptible hexaploid spring wheat cultivars Kenyon and Chinese Spring; and (iii) a complete set of Chinese Spring monosomic lines, a monotelosomic 3AS line and lines ditelosomic for 2AS, 2AL, 3AS, and 3AL. The cytogenetic stocks were supplied by Dr. A. Limin, Department of Plant Sciences, University of Saskatchewan, Saskatoon, SK, and Dr. G. Kimber and Dr. E.R. Sears, Department of Agronomy, University of Missouri, Columbia, MO.

F1 and F2 generations of the crosses Red Chief x Kenyon, Hadden x Kenyon, and 86ISMN 2137 x Kenyon, a doubled haploid (DH) population from cross 86ISMN 2137 x Kenyon, and random inbred line (RIL) populations from crosses between all five resistant winter wheat genotypes and Kenyon were tested in the inheritance study. The RIL populations were produced by F2–derived single seed descent and evaluated in two or more of the F5 to F9 generations. For the allelism study, individual resistant lines with a spring growth habit were selected from each RIL population and crossed in all possible combinations without reciprocals. F1 and F2 generations of these crosses plus crosses Red Chief x 86ISMN 2137 and Hadden x 86ISMN 2137, and DH populations and randomly selected F2:3 families from crosses Hadden x 81IWWMN 2095, Red Chief x Coker 76-35, Hadden x Missouri Queen, and Missouri Queen x Coker 76-35 were tested. DH populations were produced by the maize-hybridization method as described by Ma et al. (1999).

In the cytogenetic study, Chinese Spring, monosomic plants of each of the 21 monosomic lines and the monotelosomic 3A line were tested for seedling reaction to SNB. A few heads of monosomic plants of each line were bagged before anthesis to provide known selfed seeds of each line for use in subsequent crosses. Crosses were made between monosomic plants of each monosomic line and Red Chief, with the monosomic plants as the female parent. Monosomic F1 plants from potential critical crosses were selected and bagged to produce F2 populations. Lines ditelosomic for the long arm and for the short arm of potential critical chromosomes were crossed with Red Chief. The parental and F1 generations of these crosses were tested for disease reaction at the seedling stage. In each test, the chromosomal configurations of the aneuploid plants were determined by counting the root-tip chromosome number as described by Dvorak (1971).

Disease Testing
A single pycnidial isolate of S. nodorum, originating from an infected wheat plant from Kelvington, SK, was used throughout this study. Culture of the fungus followed the methodology described by Ma and Hughes (1995). After about 7 d when the pycnidia had produced pink cirrhi, a spore suspension was prepared at the concentration of 3.75 x 106 spores per mL and 0.4 mL Tween 20 (polyxyethlene sorbitan monolaurate) was added per liter of spore suspension.

All disease tests were conducted in a growth room at a temperature regime of 21°C (light)/18°C (dark) and a 16-h photoperiod. Seed was pregerminated for 2 d in Petri dishes on filter paper moistened with 10 µL mL–1 gibberellic acid (GA3). Germinating seeds were sown in 15-cm-diameter by 15-cm-deep pots containing a soilless mix (Redi-Earth, W.R. Grace & Co. of Canada Ltd., Ajax, ON, Canada).

Disease testing of each population was conducted by a completely randomized design. For RIL and DH populations, 20 plants from each line were planted in two pots with 10 plants per pot. For F1 and F2 generations, 20 to 30 F1 and 200 to 400 F2 seeds were planted in pots, 10 plants per pot. In each test, the appropriate resistant parents were grown as resistant checks and cultivar Kenyon or Chinese Spring as the susceptible check.

Seedlings were inoculated at the three-leaf stage by spraying the leaves with inoculum with a hand sprayer until runoff. After inoculation, the plants were placed in a moist chamber for 48 h under continuous leaf wetness and the same light and temperature conditions as the growth room and then returned to the growth room benches.

The third leaf of each plant was rated for SNB lesion type seven days after inoculation using a 1–5 disease scale for the inheritance and allelism studies (Fig. 1) . The classes of the 1-to-5 rating scale were defined as 1 = pinpoint dark-brown lesions without chlorosis; 2 = small lesions with very little necrosis or chlorosis; 3 = chlorotic lesions or necrotic lesions completely surrounded by a chlorotic ring; 4 = lesions completely surrounded by chlorotic zones, some of the lesions coalescing; and 5 = extensive chlorosis and large necrotic lesions. Ratings 1 and 2, indicating restricted lesion development, were considered to represent resistant reactions, while ratings 3-5 were considered susceptible since in these reactions there was little or no restriction to the development of chlorosis. Segregating lines in RIL populations were identified by the occurrence of various disease reactions and a 1 resistant: 3 susceptible ratio among the 20 individual plants rated (assuming single recessive gene control of resistance). In the cytogenetic study, a 0-to-9 disease rating scale developed by Ma and Hughes (1995) was used to obtain better differentiation of disease reactions because Chinese Spring is not as susceptible as Kenyon and only F1 and F2 populations were tested. Ratings 0 to 3, 4 to 5, and 6 to 9 were considered resistant, intermediate, and susceptible reactions, respectively. The ratio of resistant to susceptible plants in each segregating population was tested for goodness-of-fit to different genetic models by the chi-square statistic.



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  		Fig. 1. The 1-to-5 rating scale for seedling disease reaction to Stagonospora nodorum blotch on wheat leaves. Ratings 1 to 2 represent a resistant reaction.

 

   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Inheritance of Seedling Resistance
For each of the five winter wheat genotypes, the segregation ratios of the RIL populations indicated that resistance to SNB was controlled by a single gene (Table 1). The DH population of 86ISMN 2137 x Kenyon segregated to fit a 1 resistant:1 susceptible ratio (Table 2), suggesting that in spring wheat 86ISMN 2137 a single gene also controlled resistance. All F1 plants of the crosses Red Chief x Kenyon, Hadden x Kenyon and 86ISMN 2137 x Kenyon were susceptible and the segregation of the F2 generation of each cross fitted a 1 resistant:3 susceptible ratio (Table 2). This indicated that single recessive genes controlled resistance in cultivars Red Chief and Hadden, and in spring wheat line 86ISMN 2137.


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  		Table 1. Segregation ratios for reaction to Stagonospora nodorum blotch (SNB) in random inbred line populations tested at the three-leaf stage under controlled environmental conditions.

 

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  		Table 2. F1 plant disease reaction and segregation of F2 populations for resistance to Stagonospora nodorum blotch (SNB) in three resistant x susceptible crosses and of the doubled haploid population from cross 86ISMN 2137 x Kenyon tested at the three-leaf stage under controlled environmental conditions.

 
Allelism of the Single Genes Carried by the Resistant Genotypes
All F1 and most F2 plants of the crosses between selected individual resistant RILs and crosses Red Chief x 86ISMN 2137 and Hadden x 86ISMN 2137 were resistant to SNB (Table 3). However, susceptible F2 plants were observed in some crosses at very low frequencies. When F3 families from these susceptible F2 plants were produced, all 20 seedlings tested for each family were resistant, indicating that the F2 parent plants were homozygous resistant and that the susceptible reaction was likely the result of misclassification. This suggested that in each cross the parents carried the same gene for resistance. Because the same results were obtained from all possible cross combinations among the five winter wheat genotypes, the resistance genes possessed by all five should be allelic. Since it has been shown that cultivars Red Chief and Hadden carried single recessive genes controlling resistance, the five winter wheat genotypes must share the same recessive gene. The F1 and F2 tests of crosses Red Chief x 86ISMN 2137 and Hadden x 86ISMN 2137 indicated that spring wheat line 86ISMN 2137 carried the same recessive gene for resistance to SNB as the resistant winter wheat genotypes (Table 3).


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  		Table 3. F1 plant reaction and segregation of F2 populations for resistance to Stagonospora nodorum blotch (SNB) in resistant x resistant wheat crosses tested at the three-leaf stage under controlled environmental conditions.

 
All doubled haploid lines and F2:3 families of crosses Hadden x 81IWWMN 2095, Red Chief x Coker 76-35, Hadden x Missouri Queen and Missouri Queen x Coker 76-35 were resistant (Table 4). Ten plants of each line–family were tested for disease reaction, a sample size which gave at least a 95% probability that susceptible phenotypes would be identified in case two genes were segregating. This provided additional evidence that the five winter wheat genotypes possess the same gene for resistance to SNB.


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  		Table 4. Segregation for resistance to Stagonospora nodorum blotch (SNB) of doubled haploid populations and randomly selected F2:3 families from four crosses between selected individual resistant random inbred lines tested at the three-leaf stage under controlled environmental conditions.

 
Chromosomal Location of the Resistance Gene
The mean disease ratings of the parental, disomic F1 and monosomic F1 plants were compared for all crosses of Red Chief with the Chinese Spring monosomic lines (Table 5). The mean rating of each monosomic F1 generation of the crosses involving mono-2A and mono-3A was significantly lower than those of the corresponding monosomic parent and the disomic F1. All monosomic F1 plants of the other crosses showed an intermediate to susceptible reaction (data not shown). These results suggested that chromosomes 2A and 3A of Red Chief each carry a gene for resistance.


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  		Table 5. Mean disomic F1 and monosomic F1 ratings of Chinese Spring A-genome monosomic lines x Red Chief crosses tested for resistance to Stagonospora nodorum blotch (SNB) at the three-leaf stage under controlled environmental conditions.

 
To verify the results obtained from the F1 tests, F2 populations derived from monosomic F1 plants of the mono-2A and mono-3A crosses were tested. The F2 plants of the mono-3A cross were resistant with the exception of two plants, but no F2 plant was as susceptible as Chinese Spring or Kenyon (Table 6). The ratings of these two F2 plants are more likely the result of misclassification than of some genetic cause. Lack of segregation for susceptibility in the F2 population supports the F1 test result that chromosome 3A in Red Chief is associated with seedling resistance. However, the F2 plants of the mono-2A cross segregated for resistance (Table 6). When the range of ratings of the mono-2A parent was used to determine the combined intermediate/susceptible class range, the F2 population segregated 56 resistant: 136 intermediate/susceptible. This ratio fit a 1 resistant: 3 intermediate/susceptible segregation ({chi}2 = 1.778, P = 0.18) and indicated that chromosome 2A was not associated with resistance.


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  		Table 6. Means and frequency distributions of plant disease ratings of the crosses Chinese Spring mono-2A x Red Chief and mono-3A x Red Chief tested for resistance to Stagonospora nodorum blotch (SNB) at the three-leaf stage under controlled environmental conditions.

 
To clarify the monosomic analysis results, ditelosomic lines Dt-2AL, Dt-2AS, Dt-3AL, and Dt-3AS, and the F1 generations of their crosses with Red Chief were tested. Lines Dt-2AL and Dt-3AL were significantly more susceptible than lines Dt-2AS and Dt-3AS, indicating that the absence of the long arm of either chromosome 2A or 3A reduced the level of susceptibility (Table 7). This result can be explained if susceptibility in Chinese Spring is assumed to be controlled by two partially dominant complementary genes, one on the long arm of chromosome 2A and the other on the long arm of chromosome 3A. The presence of dominant alleles at both loci is necessary for a susceptible reaction.


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  		Table 7. Mean F1 plant disease ratings of Chinese Spring ditelosomic lines 2AL, 2AS, 3AL and 3AS x Red Chief crosses tested for resistance to Stagonospora nodorum blotch (SNB) at the three-leaf stage under controlled environmental conditions.

 
The mean F1 rating for the Red Chief x Dt-2AL and Red Chief x Dt-3AL crosses did not differ significantly from the appropriate ditelosomic parents and indicated intermediate to susceptible reactions (Table 7). However, most F1 plants of the Dt-3AS cross were resistant and no plant was as susceptible as Chinese Spring (Table 7). These results would be expected if the long arm of chromosome 3A in Red Chief carried a gene for resistance. The F1 plants were intermediate to susceptible and the mean rating of the F1 plants of the Dt-2AS cross was significantly higher than that of the ditelosomic parent (Table 7). If, as previously suggested, the long arm of chromosome 2A in Chinese Spring carries a partially dominant gene for susceptibility, this F1 reaction can be explained by assuming that chromosome 2A in Red Chief also carries that gene for susceptibility.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The genetic study indicated that resistance to SNB in six hexaploid wheat genotypes was controlled by the same recessive gene. Single-gene resistance to SNB has been reported from only three studies, all of which were conducted at the seedling stage under controlled environmental conditions (Frecha, 1973; Ma and Hughes, 1995; Murphy et al., 2000). Comparison of these and our study, with those studies reporting resistance to be polygenically controlled, suggested several factors that could explain the different results. First, the resistance sources and genetic backgrounds used in these studies were different and showed a high level of resistance to SNB. Second, most other studies were conducted in the field at varying growth stages. The environment in the field can influence both the disease severity and the expression of resistance; as well, different genes may confer resistance at different growth stages. In the wheat-leaf rust pathosystem, in addition to seedling resistance genes that are effective throughout the life of the plant, other genes for resistance that are effective only in adult plants have been identified (Zhang and Knott, 1993). Third, the methods of assessing resistance used can significantly affect the conclusions of genetic studies. Most studies conducted in the field used moderately resistant genotypes for which only quantitative assessment methods can be used. In contrast, the host genotypes used in this study conferred a high level of resistance therefore clear differentiation between resistant and susceptible reactions was possible and thus permitted a qualitative assessment.

The monosomic F1 data suggested that chromosomes 2A and 3A in Red Chief were associated with resistance, but subsequent tests of the monosomic F1–derived F2 populations of the mono-2A and mono-3A crosses indicated that only chromosome 3A carried a gene for resistance. Tests with all possible lines ditelosomic for chromosome 2A and 3A confirmed this result and showed that the resistance gene was located on the long arm of chromosome 3A. In general, the monosomic and ditelosomic studies did not support the presence of a gene for resistance on chromosome 2A. The result obtained for the mono-2A F1 test might have been caused by incomplete expression of the partially dominant allele for susceptibility on chromosome 2A when in the hemizygous condition. Partial expression of a dominant gene when in the hemizygous condition is found commonly in monosomic analysis (McIntosh, 1987).

Since the allelism studies indicated that all resistant genotypes used in this study carried the same recessive gene for resistance, it can be concluded from the cytogenetic analysis of Red Chief that the resistance gene carried by the other genotypes is also located on chromosome 3AL. A recessive gene for resistance identified in durum wheat line S12-1 derived from T. timopheevii (Zhuk.) Zhuk. (PI 290518) was also located on chromosome 3A (Ma and Hughes, 1995). The fact that the resistance genes from durum and common wheat have been located on the same chromosome suggests that these genes may be the same gene. Preliminary allelism tests conducted as a continuation of this study have suggested that the single recessive genes found from durum and common wheat were allelic. However, since their pedigrees showed no close relationship among the genotypes studied (data not shown), the possibility that the allelic relationship results from the presence of different alleles at the same or tightly linked loci cannot be excluded.

The results of this study based on the reaction of six resistant cultivars suggest that little genetic variability exists for resistance to SNB in wheat. However, other major genes for resistance to S. nodorum have been identified. These include a dominant gene on chromosome 1B in winter wheat cultivar Atlas 66 (Kleijer et al., 1977) and a dominant gene in an Aegilops tauschii Coss. (DD) accession (Murphy et al., 2000). In addition to these genes, polygenes, which function together to control a quantitatively expressed resistance, have been located on several chromosomes in the A, B, and D genomes (Nicholson et al., 1993; Hu et al., 1996). The existence of a number of different genes for resistance provides the opportunity to pyramid resistance genes from different sources or to utilize cultivar mixtures to enhance the level and durability of resistance.

The best way to utilize the gene found in this study is to transfer it to adapted cultivars by backcrossing. However, because this gene is recessive, determination of the presence or absence of this gene in a backcross individual requires a phenotypic assay of progeny generated either by selfing or by crossing to the donor parent (Allard, 1999). Molecular markers could also be used to trace the presence of the target gene in successive backcross generations. Two RAPD markers located approximately 15 and 13.1 cM from the gene found in durum line S12-1 have been identified (Cao et al., 2001).

This study was conducted on young plants at the three-leaf stage in the greenhouse. Screening wheat seedlings by artificial inoculation in the greenhouse permits examination of a large population for resistance under uniform disease pressure. This is the preferred approach for identifying major genes in genetic studies because strong selection for resistance, which can easily be achieved in greenhouse conditions, tends to select major genes (Parlevliet, 1989). A positive correlation was found between assessments of resistance at the seedling stage and ratings of adult plants in the field (Krupinsky et al., 1972; Rufty et al., 1981; Scharen and Eyal, 1983). Whether the genotypes studied here express their resistance in the adult stage under field conditions was not investigated, but unpublished results suggest that the gene controlling seedling resistance in Red Chief and Hadden is effective throughout the life of the plant (G.R. Hughes, personal communication). Thus using one or a combination of genes for resistance to produce cultivars with a high level of resistance to SNB over several growth stages is achievable. Furthermore, because the resistance conferred by these lines is under single gene control and the genotypes produce a highly resistant phenotype, the expression of resistance should not be as sensitive to environmental factors as that of moderate resistance controlled by polygenes. This gene should function at the seedling stage in the field and reduce the initial level of infection, thereby slowing development of the SNB epidemic. Resistance breeding employing a combination of seedling testing followed by selection for high levels of resistance in the field should combine resistances controlled by both major genes and polygenes, a combination expected to be durable.


   ACKNOWLEDGMENTS
 
This research was supported by Saskatchewan Agricultural Development Fund and Western Grains Research Foundation. We thank Dr. P.J. Hucl for his critical reading of the manuscript.

Received for publication February 9, 2004.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 




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