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CROP BREEDING, GENETICS & CYTOLOGY

Resistance to Fusarium Head Blight in Winter Wheat

Heritability and Trait Associations

IFA-Tulln, Institute for Agrobiotechnology, Dep. of Biotechnology in Plant Production, Konrad Lorenz Str. 20, A-3430 Tulln, Austria

buerst{at}ifa-tulln.ac.at

	ABSTRACT

TOP ABSTRACT INTRODUCTION Materials and methods Results Discussion REFERENCES

 
Fusarium head blight (FHB) or scab caused by Fusarium Link: Fr. spp. is a widespread disease of cereals, causing significant yield losses and contaminating cereal products with mycotoxins. The complex inheritance of resistance has hampered progress in breeding resistant, agronomically adapted cultivars. To streamline breeding for FHB resistance, we estimated genetic and environmental variance components and broad-sense heritability in two winter wheat (Triticum aestivum L.) populations, determined the association of FHB resistance with other traits (flowering date, plant height, and awnedness), and determined the level of maternal effects on FHB resistance. The moderately susceptible Austrian cultivar Capo was crossed with two resistant lines, one from Hungary (UNG-226) and one from the Netherlands (SVP-72017). A hierarchical design was applied to develop recombinant F₄-derived lines. Head blight resistance was measured by visual assessment of disease symptoms in artificially inoculated, mist-irrigated field experiments during 2 yr. Artificial inoculation and mist irrigation led to reproducible FHB infections. High broad-sense heritabilities (H > 0.75) were measured for FHB resistance, allowing for considerable progress by selection. The magnitude of additive genetic variance was greater than additive x additive epistatic variance. Despite a significant negative correlation between visual FHB symptoms and plant height , the successful selection of short and FHB resistant genotypes should be feasible. In only one population, awned progeny showed slightly reduced FHB. Reciprocal effects were significant in one cross only. The development of FHB resistant cultivars should be possible by phenotypic selection under epidemic conditions, and should be largely independent of plant height, flowering date, awnedness, and genotype of the maternal parent within a cross.

Abbreviations: AUDPC, area under the disease progress curve • FHB, Fusarium head blight • H, broad sense heritabiltiy

	INTRODUCTION

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FUNGI of the group Fusarium spp. have long been recognized as pathogens of many plant species. Wheat and other small grain cereals may be attacked by Fusarium spp. on different plant organs. Infestation of the ear appears to be most critical, leading to Fusarium head blight (FHB), also known as scab. The risk of a FHB epidemic is high when natural inoculum is abundant (e.g., conidia or ascospores on crop debris on the soil surface) during warm, humid weather at flowering. Head blight of wheat is a common disease in many wheat growing regions worldwide, with increasing importance in recent years. Changes in crop management practices (minimum or reduced tillage), changes in rainfall patterns, and a low resistance level among current cultivars are considered the principal causes for severe FHB epidemics in the USA and Canada since 1993 (Dill-Macky and Jones, 1997; McMullen et al., 1997). Despite the range of species implicated in the disease, Fusarium graminearum Schwabe, F. culmorum (Wm. G. Sm.) Sacc., and F. avenaceum (Fr.:Fr.) Sacc. appear to predominate worldwide (Parry et al., 1995). The disease may cause severe losses in grain yield and grain quality. Furthermore, the most serious threat of FHB is the contamination of the harvested grain with mycotoxins.

The cultivation of genetically resistant cultivars is the most cost-effective method to control the disease. Genetic variation for resistance to FHB is well documented in wheat and its relatives (Mesterhazy, 1983, 1995; Snijders, 1990a; Saur, 1991; Wilcoxson et al., 1992; Lemmens et al., 1993; Buerstmayr et al., 1996a, b). A general review of FHB on small grains has been published by Parry et al. (1995). Breeding for resistance has been reviewed by Mesterhazy (1995) and Miedaner (1997).

In recent years, increased efforts have been devoted to FHB resistance breeding, with success reported from Hungary (Mesterhazy, 1995, 1997), China (Chen et al., 1997), USA (Rudd, 1997; Stack et al., 1997), and Canada (Gilbert et al., 1997). Heritability estimates for FHB resistance are sparse and contradictory, depending on the genetic materials and methods used. Snijders (1990b) reported broad-sense heritability of FHB resistance in F₂ single-plant populations from 0.05 to 0.89. Heritability estimates by Saur and Trottet (1992) and Singh et al. (1995) were in the range of 0.66 to 0.93 but were derived from single environments.

To date, no reports are available on genetic variances and heritability of FHB resistance in winter wheat estimated in replicated field experiments across environments. In the present study, we therefore estimated genetic and environmental variance components as well as broad-sense heritability of FHB resistance in two winter wheat populations. Furthermore, the association of FHB resistance with flowering time, plant height, and awnedness was determined because these characters are considered possibly associated with passive resistance (Mesterhazy, 1995). Finally, reciprocal effects on FHB resistance were investigated in order to clarify possible cytoplasmic inheritance (Van Ginkel et al., 1996).

	Materials and methods

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Plant Materials
The moderately susceptible winter wheat cultivar Capo, which is currently among the most popular wheat cultivars in Austria, was crossed reciprocally with each of the two resistant breeding lines UNG-226 (Population 1) and SVP-72017 (Population 2). UNG-226 possibly inherited its high level of resistance from the Chinese cultivar Sumai 3, whereas SVP-72017 originated from European winter wheats (Table 1) . A hierarchical scheme was applied to develop recombinant lines. The seed from individual F₂ plants was sown in F₃ rows, from which two random single plants were advanced to the F₄. Two random plants were harvested in each F₄ family. These F_4:5 lines were tested in a field trial during 1995–1996. From every F_4:5 line, 12 spikes were taken at random, bulked, and used for sowing the field trials during 1996–1997 (F_4:6 lines). In total, Population 1 had 328 lines tracing to 82 F₂ plants, and Population 2 had 272 lines tracing to 68 F₂ individuals. The initial crosses were made in a reciprocal manner. In Population 1, 140 lines had UNG-226 and 188 lines had Capo as the female parent, and in Population 2, 108 lines had SVP-72017 and 164 had Capo as the female parent.

Inoculum and Inoculation Procedure
Inoculum was prepared as described by Snijders and Van Eeuwijk (1991). A mixture of wheat and oat kernels (3:1 v/v) was soaked overnight in water and then autoclaved and inoculated with the Fusarium culmorum strain IPO 39-01 (Snijders and Van Eeuwijk, 1991). The mixture was then incubated for 2 wk at 25°C followed by 3 wk at 5°C in the dark, leading to production of macroconidia. Macroconidia were washed off the colonized grains with deionized water. Spore concentration was determined with a Bürker-Türk counting chamber and adjusted to the desired spore concentration of 1.5 x 10⁴ spores mL^-1 with deionized water. The aggressiveness of the inoculum was monitored with a Petri-dish infection test at the beginning and at the end of the inoculation period as described by Lemmens et al. (1993). This test proved that the aggressiveness of the inoculum remained constant during the inoculation period (data not shown).

Inoculations were performed on each plot when 50 % of the plants had reached anthesis, and repeated 2 d later. Using a motor driven back-pack sprayer, we sprayed 50 mL inoculum onto the heads. Neighboring plots were protected by a plastic shield. Inoculations were carried out in the evenings on alternate days. An automated mist-irrigation system maintained humidity and kept the plants wet for 20 h after inoculation. Leaf wetness was monitored by conductivity measurement. When leaf wetness dropped below a preset value, the system started automatically, applying a 10-s pulse of water.

AUDPC as a Measure of Visual FHB Symptoms
In each plot, the percentage of visually infected spikelets was estimated according to a linear 0 (no disease) to 4 (100% infected spikelets) scale. Scoring was between 0 and 1 in 0.1-scale increments, and between 1 and 4 in 0.5 intervals. Disease symptoms were scored 10, 14, 18, 22, and 26 d after inoculation. An area under the disease progress curve (AUDPC) was calculated for each plot and used for further statistical analysis (Eq. [1]).

(1)

where y_i is the score of visually infected spikelets on the ith day and x_i is the day of the ith observation, and n is the total number of observations (modified from Shaner and Finney, 1977).

Other Traits
The number of days from 1 May to 50% anthesis was recorded. At the beginning of grain ripening, plant height was measured from the soil surface to the top of the heads, excluding awns. Every line was classified as awned, awnless, or heterogeneous for awned and awnless plants. The ratio of awned:heterogeneous:awnless F₄ derived lines was 133:54:141 and 113:67:92 for Populations 1 and 2, respectively.

Statistical Analysis
Analyses of variance were calculated by the GLM procedure of SAS (SAS Institute, 1989), assuming all factors random. The form of the analysis of variance and the associated mean square expectations were derived from Nyquist (1991). F-tests were performed applying Satterthwaite's rule (Snedecor and Cochran, 1980).

The genetic variance among F₄-derived lines (²_G) was partitioned into genetic variance components according to Nyquist (1991), as follows, for additive (²_A) and additive by additive epistatic (²_AA) variances.

The coefficients for dominance variance (²_D) are small when evaluating F₄-derived lines; thus, ²_D was considered negligible and was included in the residual term (). Estimates of genetic variance components were solved by equating observed mean squares to their genetic expectations and solving for the genetic variance components by least square procedures (Elias et al., 1989; Nyquist, 1991). The standard errors of the variance components were estimated according to Searle (1971). From the genetic variance among F₄-derived lines (²_G), we estimated heritability on a line-mean basis by . Confidence intervals for heritability were calculated according to Knapp et al. (1985). The effects of awnedness and reciprocal effects on FHB severity were tested by one-way ANOVAs based on F₄-derived line means. Genotypic and phenotypic correlation coefficients were calculated by the PLABSTAT program (Utz, 1991) from entry means.

	Results

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Population 1 showed more variation in AUDPC, plant height, and flowering date than did Population 2 (Fig. 1 ; Tables 2 and 3) . The populations had similar mean values and both were skewed towards susceptibility, and transgressive segregates were found in both directions (Table 2 and Fig. 1). However, transgressive segregates were statistically significant only in the direction of susceptibility. Genetic variance among F₄-derived lines (²_G) was highly significant for AUDPC, plant height, and flowering time in both populations. Significant variation was also observed among F₄-derived progenies within F₃ families. Interactions of genotypes with years were also significant in some cases, but these variance components were generally smaller than those for genotype effects. In Population 1, the genetic variance for AUDPC was three times larger than in Population 2. Error variance was also three times larger in Population 1 than in Population 2. Additive genetic variance was more important than additive x additive epistatic variance for AUDPC in both populations (Table 4) . Additive and epistatic variance components were similar for plant height and flowering time in Population 1. On the contrary, plant height in Population 2 was controlled mainly by additive x additive epistatic interaction, and for flowering time additive and epistatic effects were of similar importance.

View larger version (48K): [in this window] [in a new window]   Fig. 1 Distribution of F4-derived winter wheat lines for area under the disease progress curve (AUDPC) after artificial inoculation with F. culmorum in Population 1 (A) and Population 2 (B)

View this table: [in this window] [in a new window]   Table 4 Additive (2A) and additive by additive (2AA) interaction variances and their standard errors for area under the disease progress curve (AUDPC), plant height and flowering time for two winter wheat populations after artificial inoculation with F. culmorum in 2 yr

In both populations, plant height was negatively correlated with AUDPC (Table 6) . This relationship is illustrated in Fig. 2 . The significant correlation coefficient depends mainly on the fact that none of the tall genotypes (>100 cm) were severely diseased. The correlation between flowering date and AUDPC was significant in Population 1 only.

View larger version (33K): [in this window] [in a new window]   Fig. 2 Scatter plot of area under the disease progress curve (AUDPC) versus plant height for winter wheat after inoculation with F. culmorum for Population 1 (A) and Population 2 (B)

	Discussion

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Variation of FHB symptoms as measured by AUDPC was clearly quantitative, and in both populations significant genetic variation for FHB severity was present. The continuous distribution of the AUDPC values, and the presence of significant variation between pairs of F₄-within-F₃) lines indicate that FHB resistance in these populations is most likely controlled by a polygenic system. This is in agreement with earlier studies (Singh et al., 1995; Van Ginkel et al., 1996; Ban and Suenaga, 1998). Investigations on the chromosomal location of resistance genes also revealed that several chromosomes are involved in FHB resistance (Grausgruber et al., 1998; Buerstmayr et al., 1999) and furthermore, several quantitative trait loci for FHB resistance were detected by Waldron et al. (1999). Transgressive segregates were observed in both populations indicating that all parents, including the moderately susceptible Capo, carry positive and negative alleles for FHB resistance. Transgressive segregates were reported by Snijders (1990c) and Singh et al. (1995), who also found significant transgressive segregation towards susceptibility only.

For FHB resistance, additive genetic variance predominated in both populations. Therefore, conventional pedigree techniques should be effective for selecting improved genotypes. Snijders (1990c) carried out a study with F₁ and F₂ populations of a 10-parent half-diallel and concluded that significant additive gene effects occurred more frequently and were larger than dominance effects, while epistatic effects were detected in only a few crosses. On the contrary, for winter rye (Secale cereale L.), Miedaner et al. (1993) reported a limited amount of additive genetic variance compared to environmental variation. They cited this as the reason for only modest progress from selection for improved FHB resistance.

Heritability estimates were based on means over two years and two replications per year. In our study, replications were sown at separate times and thus replication effects were confounded with sowing time effects and possibly biased upward relative to spatial block effects. Furthermore, the error variance may include genotype x sowing time interactions in addition to residual effects. Population 1 had considerably more variation in flowering time leading to a longer inoculation period than Population 2. Therefore, Population 1 was exposed to more variation in weather conditions during the inoculation period, resulting in less constant infection and hence larger error and interaction variances. The heritability values for FHB severity, as measured by AUDPC, were surprisingly high in both populations. These high heritabilities were achieved with artificial inoculation and controlled humidity and using parents that differed for AUDPC. Heritability estimates of this magnitude, and the predominance of additive genetic variance indicate that progenies with improved AUDPC could be selected from these populations.

For breeding applications involving large numbers of genotypes, five successive FHB readings might not be practical. For one single visual head blight reading either on day 22 (OBS-22) or 26 (OBS-26) after inoculation, heritability values were obtained similar to AUDPC. Correlation coefficients between OBS-22 or OBS-26 and AUDPC were high (r > 0.95). Therefore, a single FHB reading 22 to 26 d after inoculation should be sufficient for the successful selection of improved lines. Singh et al. (1995) measured FHB resistance by visual disease observation and reported heritabilities ranging from 0.66 to 0.93. They used replicated single-spike inoculations in the field to evaluate F₆ recombinant inbred populations from crosses involving `Frontana' as the resistant parent. Similarly, Saur and Trottet (1992) reported heritability estimates in the range of 0.8 to 0.9 for visual FHB symptoms using spray inoculations. These heritability estimates were derived from single-environment experiments and are likely inflated by genotype x environment interaction. Snijders (1990b) reported heritability estimates from 0.05 to 0.89, with large standard errors, for visual FHB symptoms on a single-plant basis in several F₂ populations developed from 10 Dutch winter wheats. In the subsequent F₃ generation, Snijders (1990c) calculated realized heritabilities ranging from 0 to 0.96. Unfortunately, the two types of heritability estimates were not correlated. Single-plant selection for FHB resistance was apparently not effective. Miedaner et al. (1993) estimated broad-sense heritabilities in winter rye experiments across 2 yr using an approach similar to our study. He also obtained similar heritability estimates of 0.64 to 0.85 for average visual disease rating.

Heritabilities for plant height and flowering date were high. This is in good agreement with published reports (Sidwell et al., 1978; Nanda et al., 1981; Teich, 1984). Population 1 showed larger genetic variances for AUDPC as well as for plant height and flowering time than Population 2. This is not surprising as the parents of Population 1 were more divergent than those for Population 2. In both populations the correlation between plant height and AUDPC was negative (Fig. 2). Lines exceeding 100 cm in plant height were generally considered resistant in both populations. Among the shorter genotypes (<80 cm), some resistant lines (<10 AUDPC units) could be found. The lines with the least FHB symptoms were somewhat taller (80–100 cm), however. The negative relation between FHB symptoms and plant height could either be due to genetic effects (linkage or pleiotropic effects) but more likely to effects of the microenvironment. Despite mist irrigation for humidity control, the heads of taller plants may dry faster and could therefore be exposed to less humidity and wetness than those of short plants, leading to a bias in the FHB resistance measurement. Mesterhazy (1995) also reported that short plant types tended to be more susceptible to FHB than tall ones under natural infection conditions. He concluded that plant height provides a passive resistance mechanism. The weak (Population 1) or no (Population 2) correlation between AUDPC and flowering time allows the selection of FHB resistant genotypes largely independent of flowering time. Reciprocal effects on AUDPC were of minor importance. This is in agreement with the results of Van Ginkel et al. (1996) who also found only small maternal effects. It seems irrelevant which parent is used as male or as female for FHB resistance breeding.

The development of FHB resistant cultivars should be possible by phenotypic selection under epidemic conditions. Selection should be largely independent of plant height, flowering date, awnedness, and the maternal genotype within a cross.SAS Institute Inc 1989

	ACKNOWLEDGMENTS

 
We thank Dr. A. Mesterhazy (CRI, Szeged) and Dr. C.H.A. Snijders (CPRO-DLO, Wageningen) for supplying the resistant lines. For excellent technical help we thank Mr. M. Fidesser. We are very grateful to Dr. W. Nyquist (Purdue Univ.) and Dr. H.F. Utz (Univ. Hohenheim) for statistical advice and to Dr. R. Dill-Macky (Univ. Minnesota), Dr. W. Link (Univ. Goettingen) and Dr. J. Vollmann (BOKU Vienna) for critically reading the manuscript. We gratefully acknowledge the Austrian Science Fund (FWF) for financial support, project number P 9190-BIO.

Received for publication May 12, 1999.

	REFERENCES

TOP ABSTRACT INTRODUCTION Materials and methods Results Discussion REFERENCES

 

• Ban, T., and K. Suenaga. 1998. Genetic analysis of resistance to Fusarium head blight caused by Fusarium graminearum in wheat. p. 192–196. In A.E. Slinkard (ed.) Proc. Intl. Wheat Genetics Symp., 9th, Saskatoon, SK. 2–7 Aug. 1998. Univ. of Saskatchewan Extension, Saskatoon.
• Buerstmayr H., Lemmens M., Grausgruber H., Ruckenbauer P. Scab resistance of international wheat germplasm. Cereal Res. Comm. 1996;24:195-202 a.
• Buerstmayr H., Lemmens M., Patschka G., Grausgruber H., Ruckenbauer P. Head blight (Fusarium spp.) resistance of wheat cultivars registered in Austria. Die Bodenkultur 1996;47:183-190 b.
• Buerstmayr H., Lemmens M., Fedak G., Ruckenbauer P. Back-cross reciprocal monosomic analysis of Fusarium head blight resistance in wheat (Triticum aestivum L.). Theor. Appl. Genet. 1999;98:76-85.
• Chen, P., D. Liu, and W. Sun. 1997. New countermeasures of breeding wheat for scab resistance. p. 59–65. In J. Dubin, et al. (ed.). Fusarium head scab: Global status and future prospects. Proc. Workshop, El Batan, Mexico. 13–17 Oct. 1996. CIMMYT, Mexico, D.F.
• Dill-Macky R., Jones R.K. The effect of previous crops and tillage on Fusarium head blight of wheat. Cereal Res. Comm. 1997;25:711-712.
• Elias E., Cantrell R.G., Hosford R.M. Heritability of resistance to tan spot in durum wheat and its association with other agronomic traits. Crop Sci. 1989;29:299-304.[Abstract/Free Full Text]
• Gilbert, J., G. Fedak, J.D. Procunier, T. Aung, and A. Tekauz. 1997. Strategies for breeding resistance to Fusarium head blight in Canadian spring wheat. p. 47–51. In J. Dubin, et al. (ed.). Fusarium head scab: Global status and future prospects. Proc. Workshop, El Batan, Mexico. 13–17 Oct. 1996. CIMMYT, Mexico, D.F.
• Grausgruber H., Lemmens M., Buerstmayr H., Ruckenbauer P. Chromosomal location of Fusarium head blight resistance and in vitro toxin tolerance in wheat using the Hobbit sib (Triticum macha) chromosome substitution lines. J. Genet. Breed. 1998;52:173-180.
• Knapp S.J., Stroup W.W., Ross W.M. Exact confidence intervals for heritability on a progeny mean basis. Crop Sci. 1985;25:192-194.[Abstract/Free Full Text]
• Lemmens M., Buerstmayr H., Ruckenbauer P. Variation in Fusarium head blight susceptibility of international and Austrian wheat breeding material. Die Bodenkultur 1993;44:65-78.
• McMullen M., Jones R., Gallenberg D. Scab of wheat and barley: A re-emerging disease of devastating impact. Plant Dis. 1997;81:1340-1348.
• Mesterhazy A. Breeding wheat for resistance to Fusarium graminearum and Fusarium culmorum. Z. Pflanzenzüchtung 1983;91:295-311.
• Mesterhazy A. Types and components of resistance to Fusarium head blight. Plant Breeding 1995;114:377-386.
• Mesterhazy, A. 1997. Breeding for resistance to Fusarium head blight of wheat. p. 79–85. In J. Dubin, et al. (ed.). Fusarium head scab: Global status and future prospects. Proc. Workshop, El Batan, Mexico. 13–17 Oct. 1996. CIMMYT, Mexico, D.F.
• Miedaner T. Breeding wheat and rye for resistance to Fusarium diseases. Plant Breeding 1997;116:201-220.
• Miedaner T., Borchardt D.C., Geiger H.H. Genetic analysis of inbred lines and their crosses for resistance to head blight (Fusarium culmorum, F. graminearum) in winter rye. Euphytica 1993;65:123-133.
• Nanda G.S., Hazarika G.N., Gill K.S. Inheritance of heading date, plant height, ear length and spikelets per spike in an intervarietal cross of wheat. Theor. Appl. Genet. 1981;60:167-171.
• Nyquist W.E. Estimation of heritability and prediction of selection response in plant populations. Crit. Rev. Plant Sci. 1991;10:235-322.
• Parry D.W., Jenkinson P., McLeod L. Fusarium ear blight (scab) in small grain cereals - a review. Plant Pathology 1995;44:207-238.
• Rudd, J. 1997. Breeding spring wheat for scab resistance in the United States. p. 66–70. In J. Dubin, et al. (ed.). Fusarium head scab: Global status and future prospects. Proc. Workshop, El Batan, Mexico. 13–17 Oct. 1996. CIMMYT, Mexico, D.F.
• SAS Institute Inc. 1989. SAS/STAT user's guide, Version 6, 4th Edition, Cary, NC.
• Saur L. Recherche de géniteurs de résistance à fusariose de l'épi causée par Fusarium culmorum chez le blé et les espèces voisines. Agronomie 1991;11:535-541.
• Saur L., Trottet M. Héritabilité de la résistance à la fusariose de l'épi et sélection récurrente dans une population de blé tendre. Agronomie 1992;12:297-302.
• Schroeder H.W., Christensen J.J. Factors affecting the resistance of wheat to scab caused by Gibberella zeae. Phytopathology 1963;53:831-838.[Web of Science]
• Searle S.R. Linear models. New York: John Wiley & Sons, 1971.
• Shaner G., Finney R.A. The effect of nitrogen fertilization on the expression of slow-mildewing resistance in Knox wheat. Phytopathology 1977;67:1051-1056.[Web of Science]
• Sidwell R.J., Smith E.L., McNew R.W. Heritability and genetic advance of selected agronomic traits in a winter wheat cross. Cereal Res. Comm. 1978;6:103-111.
• Singh R.P., Ma H., Rajaram S. Genetic analysis of resistance to scab in spring wheat cultivar Frontana. Plant Dis. 1995;79:238-240.
• Snedecor, G.W., and W.G. Cochran. 1980. Statistical Methods. 7th ed. Iowa State Univ. Press. Ames, IA.
• Snijders C.H.A. Genetic variation for resistance to Fusarium head blight in bread wheat. Euphytica 1990;50:171-179 a.[Web of Science]
• Snijders C.H.A. The inheritance of resistance to head blight caused by Fusarium culmorum in winter wheat. Euphytica 1990;50:11-18 b.[Web of Science]
• Snijders C.H.A. Response to selection in F2 generations of winter wheat for resistance to head blight caused by Fusarium culmorum. Euphytica 1990;50:163-169 c.
• Snijders C.H.A., Van Eeuwijk F.A. Genotype x strain interactions for resistance to Fusarium head blight caused by Fusarium culmorum in winter wheat. Theor. Appl. Genet. 1991;81:239-244.[Web of Science]
• Stack R.W., Frohberg R.C., Casper H. Reaction of spring wheats incorporating Sumai#3-derived resistance to inoculation with seven Fusarium species. Cereal Res. Comm. 1997;25:667-671.
• Teich A.H. Heritability of grain yield, plant height and test weight of a population of winter wheat adapted to Southwestern Ontario. Theor. Appl. Genet. 1984;68:21-23.
• Utz, H.F. 1991. PLABSTAT a computer program for statistical analysis of plant breeding experiments. Institute of Plant Breeding, Seed Science and Population Genetics, Univ. of Hohenheim, Germany.
• Van Eeuwijk F.A., Mesterhazy A., Kling C.I., Ruckenbauer P., Saur L., Buerstmayr H., Lemmens M., Keizer L.C.P., Maurin N., Snijders C.H.A. Assessing non-specificity of resistance of wheat to head blight caused by inoculation with European strains of Fusarium culmorum, F. graminearum and F. nivale, using a multiplicative model for interaction. Theor. Appl. Genet. 1995;90:221-228.[Web of Science]
• Van Ginkel M., Van der Schaar W., Yang Z.P., Rajaram S. Inheritance of resistance to scab in two cultivars from Brazil and China. Plant Dis. 1996;80:863-867.
• Waldron B.L., Moreno-Sevilla B., Anderson J.A., Stack R.W., Frohberg R.C. RFLP mapping of QTL for Fusarium head blight resistance in wheat. Crop Sci. 1999;39:805-811.[Abstract/Free Full Text]
• Wilcoxson R.D., Busch R.H., Ozmon E.A. Fusarium head blight resistance in spring wheat cultivars. Plant Dis. 1992;76:658-661.

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