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Published online 20 May 2008
Published in Crop Sci 48:1107-1116 (2008)
© 2008 Crop Science Society of America
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Evaluation of Seedling Resistance to Tan Spot and Stagonospora nodorum Blotch in Tetraploid Wheat

C. G. Chua, T. L. Friesenb, J. D. Farisb and S. S. Xub,*

a Dep. of Plant Sciences, North Dakota State Univ., Fargo, ND 58105
b USDA-ARS, Northern Crop Science Laboratory, Fargo, ND 58105. Mention of trade names or commercial products in this article is solely for the purpose of providing specific information and does not imply recommendation or endorsement by the U.S. Department of Agriculture

* Corresponding author (steven.xu{at}ars.usda.gov).


   ABSTRACT
TOP
 NOTES
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
Tetraploid durum wheat (Triticum turgidum L. subsp. durum), an important cereal used for making pasta products, is more vulnerable to various wheat diseases than bread wheat (T. aestivum L.). To identify resistant sources useful for improving durum resistance to tan spot [caused by Pyrenophora tritici-repentis (Died.) Drechs.] and Stagonospora nodorum blotch (SNB) [caused by Phaeosphaeria nodorum (E. Müller) Hedjaroude], we evaluated 688 accessions belonging to T. turgidum L. subspecies T. carthlicum, T. polonicum, T. turgidum, T. dicoccum, and T. turanicum for their seedling resistance to P. tritici-repentis and P. nodorum. Accessions were inoculated with a P. tritici-repentis race 1 isolate (Pti2) and a mixture of three diverse isolates of P. nodorum (LDNSn4, BBCSn5, and Sn2000). Then 206 accessions with low and intermediate disease reaction to either of the inocula were further evaluated for reactions to P. tritici-repentis and P. nodorum and for sensitivity to host-selective toxins produced by the two pathogens. Data showed that 25 and 132 accessions had high levels of or partial resistance to tan spot and SNB, respectively, with 10 accessions, including T. dicoccum and T. turgidum, showing resistance to both diseases. The resistant accessions identified in this study would be particularly useful for developing durum wheat germplasm resistant to tan spot and SNB due to their semidomesticated characteristics and same genomic constitutions as durum wheat.

Abbreviations: CIMMYT, International Maize and Wheat Improvement Center • HST, host selective toxin • QTL, quantitative trait locus • SHW, synthetic hexaploid wheat • SNB, Stagonospora nodorum blotch


   INTRODUCTION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
TAN SPOT AND Stagonospora nodorum blotch (SNB), caused by the fungi Pyrenophora tritici-repentis (Died.) Drechs. and Phaeosphaeria nodorum (E. Müller) Hedjaroude [anamorph: Stagonospora nodorum (Berk.) Castellani & E. G. Germano], respectively, are two destructive foliar diseases of common wheat (Triticum aestivum L.) (2n = 6x = 42) and durum wheat (T. turgidum L. ssp. durum) (2n = 4x = 28). They both can cause yield losses as high as 50% during an epidemic (Riede et al., 1996; Fried and Meister, 1987). In recent years, tan spot and SNB have become quite common in many wheat production regions primarily because of climate changes and reduced tillage practices in many wheat growing regions of the world (Xu et al., 2004). Tan spot was identified as the most prevalent disease of wheat in Canada in 2003 (Tekauz et al., 2004), and Perello et al. (2003) indicated that tan spot has become more destructive in the southern Cone region of South America, including Argentina, Brazil, Chile, Paraguay, and Uruguay. Stagonospora nodorum blotch has been reported to occur in many parts of the world (Leath et al., 1993) and has become more common and important in some wheat production regions (DePauw, 1995).

Growing resistant cultivars is considered the most effective strategy for controlling tan spot and SNB. Unfortunately, the majority of current durum and bread wheat cultivars are susceptible to both diseases due to their narrow genetic base (Lamari et al., 2005). Efforts to search for sources of resistance have been reported in a number of studies (Riede et al., 1996; Xu et al., 2004; Singh et al., 2006a,b; Wicki et al., 1999). Although complete resistances or immunity to the two diseases have not been identified, a high level of partial resistance to tan spot and SNB has been identified in synthetic hexaploid wheat (SHW) (Xu et al., 2004), bread wheat (Rees and Platz, 1990; Singh et al., 2006a,b), and its relative species such as T. timopheevii (Ma and Hughes, 1995), T. monococcum (Ma and Hughes, 1993), Aegilops tauschii (Ma and Hughes, 1993), Ae. speltoides (Ecker et al., 1990a), and Ae. longissima (Ecker et al., 1990b). However, high levels of resistance to both tan spot and SNB have not been identified in durum wheat germplasm. Xu et al. (2004) observed that almost all of the 35 durum wheat cultivars and breeding lines used as parents of International Maize and Wheat Improvement Center (CIMMYT) SHW lines are susceptible to the two diseases. In their recent studies, Singh et al. (2006a,b) evaluated a large number of wheat germplasm for resistance to tan spot and SNB and found no durum genotypes with a high level of resistance to both diseases.

Resistant sources of hexaploid wheat and wild relatives could be potentially used for durum wheat breeding. However, introgression of the resistance from hexaploid wheat to tetraploid durum wheat may not be always effective because the inheritance of complete resistance to tan spot and SNB in wheat, in most cases, is quantitative (Cao et al., 2001; Faris et al., 1997; Faris and Friesen, 2005; Friesen and Faris, 2004; Liu et al., 2004b). If gene interactions between the A or B genomes and the D genome contribute to some extent to resistance, or the major quantitative trait loci (QTLs) for resistance are located in D-genome chromosomes, introgression of the resistance could not be accomplished using conventional breeding approaches. Introgression of the resistance genes or major QTLs from alien species requires substantial efforts to induce homeologous recombination through chromosome engineering. Thus, the most useful source of tan spot and SNB resistance for durum wheat may be from other tetraploid wheat subspecies.

We recently evaluated 172 wild emmer accessions from Israel and identified 34 accessions with resistance to both tan spot and SNB (Chu et al., 2008), suggesting that other tetraploid wheat subspecies may possess resistance to the two diseases. This discovery motivated us to further evaluate the germplasm collections in five other tetraploid wheat subspecies, including T. carthlicum, T. dicoccum, T. polonicum, T. turanicum, and T. turgidum. Compared with wild emmer, these five subspecies are all in cultivated form, and their resistance, if identified, can be transferred into durum wheat using conventional breeding approaches.

The fungi causing tan spot and SNB both produce host selective toxins (HSTs). It has been demonstrated that HSTs are virulence factors and that disease severity usually correlates with sensitivity to the HSTs produced by the fungi. Host sensitivity to Ptr ToxA, a well-characterized toxin produced by P. tritici-repentis, has been found to be associated with disease susceptibility to P. tritici-repentis race 2 (Friesen et al., 2003; Lamari and Bernier, 1991). The dominant gene Tsn1 controls sensitivity to Ptr ToxA, which is located on wheat chromosome arm 5BL (Faris et al., 1996). Genotypes without Tsn1 are insensitive to the toxin (Anderson et al., 1999). By using partially purified SnTox1, a toxin predominantly produced by P. nodorum, Liu et al. (2004a,b) identified a gene, Snn1, conferring toxin sensitivity on chromosome arm 1BS, which explained as much as 58% of the phenotypic variation in SNB disease reaction. Friesen et al. (2006) indicated that the gene encoding Ptr ToxA in P. tritici-repentis was transferred from P. nodorum in a very recent horizontal gene transfer event. They noted a strong correlation between SnToxA sensitivity and SNB disease reaction. Therefore, the sensitivity of genotypes to major HSTs is an important factor in germplasm evaluation for resistance to both SNB and tan spot.

In this study, we attempted to identify new sources of tan spot and SNB resistance that can be easily used for durum wheat by evaluating a large number of accessions belonging to five cultivated tetraploid wheat subspecies, including T. carthlicum, T. dicoccum, T. polonicum, T. turanicum, and T. turgidum for reactions to P. tritici-repentis and P. nodorum and sensitivity to the HSTs produced by the two fungi.


   MATERIALS AND METHODS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS AND DISCUSSION
 REFERENCES
 
Plant Materials
A total of 688 accessions of cultivated tetraploid wheat were evaluated (Table 1 ). The collection consists of 97 T. turgidum L. subsp. carthlicum (Nevski) Á. Löve & D. Löve, 81 T. turgidum L. subsp. polonicum (L.) Thell, 200 T. turgidum L. subsp. turgidum (L.) Thell, 200 T. turgidum subsp. dicoccum (Shrank ex Schübler) Thell., and 110 T. turgidum L. subsp. turanicum (Jakubz.) Á. Löve & D. Löve accessions. The original seeds were kindly provided by Dr. Harold Bockelman USDA-ARS, National Small Grain Research Facility, National Small Grain Collection, Aberdeen, ID. In addition, the CIMMYT SHW line W-7976 and the hard red spring wheat cultivar Grandin were used as the resistant and susceptible checks, respectively.


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  		Table 1. List of 688 tetraploid wheat (Triticum turgidum L. ssp.) accessions evaluated in this study.{dagger}

 
Disease Screening Procedures
A randomized complete block design was used. All cultivated tetraploid accessions were first evaluated for reaction to P. tritici-repentis and P. nodorum, respectively, and then accessions with low or intermediate reaction types to either pathogen were selected and evaluated in two separate two-replicate experiments. Evaluation of reactions to P. tritici-repentis and P. nodorum were conducted under controlled greenhouse and growth chamber conditions using experimental procedures described by Friesen et al. (2003) and Xu et al. (2004). A slight modification of the evaluation procedure is that in the first round of evaluation, both the resistant and susceptible checks were planted in three cones on the right border of each RL98 tray; the remaining cones around the border as well as cones inside were all planted with accessions to be tested.

The isolate Pti2 of P. tritici-repentis race 1 was used to produce inocula for evaluation of resistance to tan spot. Pyrenophora tritici-repentis race 1 is the most prevalent race in North America (Ali and Francl, 2003), and it also contains virulence factors found in race 2 (Lamari et al., 2003), the second most prevalent race (Ali and Francl, 2003). The isolate Pti2 was originally collected from a wheat field in South Dakota. Disease reactions were rated 7 d postinoculation using the 1 to 5 scale lesion-type rating system developed by Lamari and Bernier (1989), with 1 being resistant, 2 moderately resistant, 3 moderately resistant to moderately susceptible, 4 susceptible, and 5 highly susceptible. Lines showing equal number of two lesion types were given an intermediate reaction type (e.g., reaction type 1 and 2 equals 1.5).

For evaluation of reaction to P. nodorum, three diverse isolates, LDNSn4, BBCSn5, and Sn2000 were used to produce conidia. Three conidial suspensions were then equally mixed before inoculation. Sn2000 was collected from a North Dakota wheat field in 1980, and it has been shown to be an aggressive isolate that produces SnTox1 (Liu et al., 2004a) and SnToxA (Friesen et al., 2006). Sn2000 has been used to screen North Dakota wheat germplasm and breeding lines. Isolates LDNSn4 and BBCSn5, collected from North Dakota and Minnesota, respectively, produce other toxins in addition to those produced by Sn2000 (Friesen et al., 2007). Therefore, the mixture of these three isolates provides a variety of virulence factors present in P. nodorum. The concentration of conidial suspensions was adjusted to 1 x 106 conidia mL–1, and plants were inoculated until runoff. The rating system used for P. nodorum is a qualitative numerical scale of 0 to 5 based on the lesion type as described in Liu et al. (2004b).

Toxin Infiltration
Toxin infiltration was done on those accessions with low disease reaction type after the first round of screening. At the two-leaf stage, plant leaves (three plants per line) were infiltrated with purified Ptr ToxA (provided by S.W. Meinhardt, Department of Plant Pathology, North Dakota State University, Fargo) and culture filtrate produced from Sn2000KO6-1, a strain generated from Sn2000 in which the SnToxA gene has been disrupted (Friesen et al., 2006). Sn2000 wild-type produces SnTox1 (Liu et al., 2004a) and SnToxA (Friesen et al., 2006), but with the disruption of ToxA gene, culture filtrates from Sn2000KO6–1 no longer contain SnToxA but still produce SnTox1 and potentially other unidentified host selective toxins. Toxin infiltration was done according to Xu et al. (2004). Leaves were evaluated 4 d after infiltration and scored as insensitive (–) or sensitive (+). Because SnToxA is functionally identical to Ptr ToxA (Friesen et al., 2006), the results from the Ptr ToxA infiltrations were considered the same as that for SnToxA infiltration.

Statistical Analysis
Statistical analysis was performed using the SAS version 9.1 (SAS Institute, 1999). Bartlett's {chi}2 was calculated to test the homogeneity of variance in different replications. The least significant difference was used to test the significance of difference between the accessions as well as the checks. The two-sample t test was used to test the difference of average disease reactions to P. tritici-repentis and P. nodorum according to the reaction to HSTs. Regression analysis was performed to evaluate the correlation between sensitivity to HSTs and average reaction to P. tritici-repentis and P. nodorum. For regression analysis, the sensitivity was converted from sensitive and insensitive to 1 and 0, respectively.


   RESULTS AND DISCUSSION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
REFERENCES
 
The evaluation data showed that different subspecies exhibited different reactions to P. tritici-repentis and P. nodorum (Table 2 ). Among the 97 T. carthlicum accessions, 42 had low or intermediate disease reactions to P. nodorum (≤2.5), but all were susceptible to tan spot. In contrast, 11 out of the 110 T. turanicum accessions had low or intermediate disease reactions to P. tritici-repentis, but no resistance to SNB was observed in this subspecies (Table 2).


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  		Table 2. Number of accessions with low or intermediate disease reaction (≤2.5) after the first round of screening in 688 tetraploid wheat (Triticum turgidum L. ssp) accessions investigated.

 
Both T. turgidum and T. dicoccum appeared to be rich sources for resistance to both tan spot and SNB, particularly in T. dicoccum, where 61 and 86 out of 200 accessions investigated showed low or intermediate disease reaction types (≤2.5) to P. tritici-repentis and P. nodorum, respectively. Furthermore, 35 accessions in T. dicoccum and 7 accessions in T. turgidum showed low to intermediate disease reactions (≤2.5) to both diseases. In total, 206 of 688 accessions had disease reaction types of less than 2.5 to either or both of the diseases in the first round of screening (Table 2). To verify the resistance, the 206 accessions were further evaluated for their reactions to P. tritici-repentis, P. nodorum, and HSTs produced by the two fungi in two additional experiments with two replications.

Reaction to Pyrenophora tritici-repentis and Ptr ToxA in Accession Subsets
After the second round of evaluation of the subset of 206 accessions inoculated with P. tritici-repentis race 1 (Pti2) in two replicates, we then calculated Bartlett's {chi}2 to test the variance homogeneity of disease reaction data from all three replications. Bartlett's {chi}2 test indicated that the variance of disease reaction from all three replications was homogeneous ({chi}2 = 3.58, P = 0.17, df = 2); thus, the data were combined (Table 3 ). Twenty-five accessions had average disease reaction types less than 2 and are considered as resistant or partially resistant. The average disease reaction types of these accessions are shown in Table 4 . Among these resistant accessions, 8, 13, and 4 were from T. turgidum, T. dicoccum, and T. turanicum, respectively. No resistance was identified among the T. carthlicum and T. polonicum accessions.


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  		Table 3. Number of resistant accessions with disease reaction type ≤2 in each tetraploid wheat subspecies (Triticum turgidum L. ssp.) when inoculating with Pyrenophora tritici-repentis and Phaeosphaeria nodorum at seedling stage after three replicates.

 

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  		Table 4. Average disease reaction to Phaeosphaeria nodorum (Sn) and Pyrenophora tritici-repentis (Ptr) and sensitivity to Ptr/SnToxA and culture filtrate (CF) of Sn2000KO6-1 in 147 tetraploid wheat (Triticum turgidum L. ssp) accessions that identified as resistant to either or both of the diseases from 206 subset accessions after three replicates.{dagger}

 
Results from Ptr ToxA infiltration in the subset show that 194 of the 206 accessions were insensitive, indicating that the majority of the accessions in the subset do not carry Tsn1. Since Tsn1 has been found to be associated with increased disease susceptibility to both tan spot and SNB (Friesen et al., 2003, 2006; Lamari and Bernier, 1991), the presence of a limited number of accessions in the subset that carry Tsn1 was likely due to the elimination of Tsn1 genotypes from the first-round evaluation. The average disease reaction type of Ptr ToxA sensitive accessions was 3.2, which is slightly higher than that of insensitive accessions (3.0), suggesting that the sensitivity to Ptr ToxA can increase the susceptibility to P. tritici-repentis. But t test results showed that the difference was not significant (Table 5 ).


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  		Table 5. Two sample t test to compare the difference of average reactions to Pyrenophora tritici-repentis and Phaeosphaeria nodorum based on the reactions to host selective toxins (HSTs) in 206 tetraploid wheat accessions investigated.

 
Sensitivity to Ptr ToxA has been reported to account for approximately 20% of the variation in tan spot disease reaction in a hexaploid wheat mapping population (Friesen et al., 2003). Xu et al. (2004) found the R2 of 0.1 for association between sensitivity to Ptr ToxA and susceptibility to P. tritici-repentis in SHW lines. The results from our study suggest that Tsn1 may have some positive effect on tan spot disease development in tetraploid wheat. The nonsignificant effect of sensitivity to Ptr ToxA on tan spot disease severity may have resulted from the genotype composites of the subset in which most of the accessions were insensitive to Ptr ToxA. Thus, the difference of tan spot reaction between Ptr ToxA sensitive and insensitive accessions may not truly reflect the effect of Tsn1 on the development of tan spot. Alternatively, as indicated by Faris and Friesen (2005), Ptr ToxA may not be a significant factor in tan spot development. They reported race-nonspecific tan spot resistance QTLs on chromosomes 1B and 3B, but there was no effect of Tsn1 on 5B. The results of this research indicate that genes other than Tsn1 are involved with resistance to tan spot in many of the accessions evaluated, which is consistent with the result from T. dicoccoides, a wild relative of tetraploid wheat (Chu et al., 2008).

Reaction to Phaeosphaeria nodorum, SnToxA and Culture Filtrate in Subset Accessions
The Bartlett's {chi}2 test showed that variance of disease reaction in the subset of 206 accessions to P. nodorum among the three replicates was homogeneous ({chi}2 = 1.26, P = 0.53, df = 2). Therefore, the disease reaction data from the three replicates were pooled and the number of accessions with average disease reactions ≤2 are shown in Table 4. A total of 132 out of 206 accessions showed resistance to SNB, with 59 accessions showing SNB disease reactions <1 (Table 4). Among these resistant accessions, 37 were T. carthlicum, 3 were T. polonicum, 21 were T. turgidum, and 71 were T. dicoccum, suggesting that these subspecies are good sources of SNB resistance. No resistance was identified from T. turanicum.

By viewing the reactions of the accessions to P. tritici-repentis and P. nodorum, we observed that five accessions each of T. turgidum (PI 210385, PI 190932, PI 190979, PI 220356, and CItr 13712) and T. dicoccum (PI 41025, PI 94634, PI 182743, PI 190922, and CItr 14133) showed average disease reactions <2 for both diseases. These would be especially useful for improving tan spot and SNB resistance simultaneously or for use as parental lines of mapping populations. The evaluation data also suggest that T. dicoccum has the largest number of accessions resistant to both tan spot (13 accessions) and SNB (71 accessions). Recently, we also found that its wild relative, T. dicoccoides, is a rich source for tan spot and SNB resistance (Chu et al., 2008). Because T. dicoccum is most closely related to T. dicoccoides, some common tan spot and SNB resistance genes may possibly exist in both subspecies.

Reaction to toxins produced by P. nodorum was found to be correlated with the SNB disease reaction in the subset of 206 accessions investigated. The average SNB disease reactions of the accessions insensitive to SnToxA was 1.6, which was significantly (t test, P < 0.0001) lower than the 3.9 found in the sensitive accessions (Table 5). Simple linear regression analysis showed that SNB disease susceptibility was significantly associated with sensitivity to SnToxA (Table 6 , R2 = 0.24, P < 0.0001). The average disease reaction (1.4) of the accessions insensitive to Sn2000KO6-1 culture filtrate was also significantly (t test, P < 0.0001) lower than that (2.3) of sensitive accessions (Table 5). Simple linear regression analysis revealed that SNB disease reactions significantly correlate with sensitivity to the culture filtrate (Table 6, R2 = 0.12, P < 0.0001).


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  		Table 6. Regression analysis to evaluate the association of sensitivity to host selective toxins with average reaction to Phaeosphaeria nodorum in 206 cultivated tetraploid wheat accessions investigated.

 
The isolate Sn2000 can predominantly produce SnTox1 (Liu et al., 2004a) and SnToxA (Friesen et al., 2006). Isolate Sn2000KO6-1 was derived from Sn2000 by disrupting the SnToxA gene (Friesen et al., 2006). Thus, the reactions of the accessions to culture filtrate of Sn2000KO6-1 would mainly reflect sensitivity to SnTox1 but potentially other unidentified toxins present in the culture filtrates. Therefore, SNB disease reactions in the tetraploid wheat accessions investigated are strongly correlated with sensitivity to SnToxA and SnTox1 or additional toxins. We obtained similar results from evaluating T. dicoccoides accessions (Chu et al., 2008). These results are consistent with the reports of Friesen et al. (2006) and Liu et al. (2004b) in hexaploid wheat, indicating the genetic control of major resistance to SNB in tetraploid wheat may be the same as that found in hexaploid wheat; that is, SNB resistance in tetraploid wheat is mainly conferred by Tsn1 on chromosome arm 5BL and Snn1 on chromosome arm 1BS.

Multiple regression analysis on the sensitivity to both SnToxA and culture filtrate of Sn2000KO6-1 with SNB disease reaction revealed an increased association between sensitivity to the HSTs and susceptibility to SNB (Table 6, R2 = 0.30, P < 0.0001), suggesting that the effects from Tsn1 (SnToxA sensitive) and Snn1 (SnTox1 sensitive) or other unidentified toxin sensitivity loci are additive. The difference of average disease reactions between the accessions insensitive to both SnToxA and Sn2000KO6-1 culture filtrate and the accessions insensitive to at least one of the HSTs is 1.0, and t test showed it to be significant at P < 0.0001 (Table 5). Thus, host insensitivity to both toxins could significantly increase its resistance to SNB, further indicating the additive effects of the SNB resistance from different genomic regions governing sensitivity to the toxins.

In summary, 688 cultivated tetraploid wheat accessions belonging to T. carthlicum, T. dicoccum, T. polonicum, T. turanicum, and T. turgidum were evaluated for their seedling resistance to tan spot and SNB. A number of accessions with resistance to either of the diseases were identified, and 10 accessions showed resistance to both diseases. In addition, almost half of the accessions we investigated were also tested for their resistance to Fusarium head blight (caused by Fusarium graminearum Schwabe [teleomorph: Gibberella zeae (Schw.) Petch]), and a few accessions of T. carthlicum and T. dicoccum resistant to tan spot and/or SNB were also showed good resistance to Fusarium head blight (Oliver et al., 2008). Therefore, the resistant tetraploid wheat accessions investigated in this study may be useful for improving durum wheat for resistance to multiple fungal diseases. Since all the accessions are currently maintained in USDA National Small Grain Research Facility, evaluation data presented in this article can provide useful information for the selection of parental lines either for practical breeding or for developing mapping populations to identify the resistance genes and their associated molecular markers.


   ACKNOWLEDGMENTS
 
The authors thank S. B. Zhong and X. W. Cai for critical review of this manuscript, H. Bockelman for providing the seeds of all tetraploid wheat, and S.W. Meinhardt for providing purified Ptr ToxA. This research was supported by USDA-ARS CRIS Projects 5442-22000-030-00D and 5442-22000-043-00D.


   NOTES
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 NOTES
ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
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Received for publication December 20, 2007.


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