Published in Crop Sci. 43:1960-1966 (2003).
© 2003 Crop Science Society of America
677 S. Segoe Rd., Madison, WI 53711 USA
CROP BREEDING, GENETICS & CYTOLOGY
Inheritance of Resistance to Fusarium Head Blight in Four Populations of Barley
Flavio Capettini*,a,
Donald C. Rasmussonb,
Ruth Dill-Mackyc,
Edward Schiefelbeinb and
Amar Elakkadc
a ICARDA/CIMMYT, Apdo. Postal 6-641, 06600 Mexico DF, Mexico
b Dep. of Agronomy and Plant Genetics, 411 Borlaug Hall, Univ. of Minnesota, St. Paul, MN 55108
c Dep. of Plant Pathology, 495 Borlaug Hall, Univ. of Minnesota, St. Paul, MN 55108
* Corresponding author (f.capettini{at}cgiar.org).
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ABSTRACT
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Fusarium Head Blight (FHB), caused by Fusarium graminearum Schwabe [(teleomorph Giberella Zeae (Schwein.)], has been a major disease problem of barley (Hordeum vulgare L.) in the U.S. Midwest since 1993. It can make a potentially profitable barley crop unusable for malting, and substantially reduce its value as a feed grain. The main cause of economic loss in malting barley is the presence of deoxynivalenol (DON) or vomitoxin, a mycotoxin produced by the fungus. The objective of this research was to investigate the inheritance of resistance to FHB by the estimation of heritability through components of variance in multiple environments. Four populations resulting from crosses between putative resistant and susceptible parents were evaluated in inoculated and mist irrigated nurseries at three locations in Minnesota from 1995 to 1997 and China in 1997. On the basis of multiple environment data, estimates of heritability for FHB ranged from 0.48 to 0.76. Heritability estimates from individual environments for FHB ranged from low to high; these estimates were likely inflated by genotype x environment (G x E) interaction. Resistance levels approximating that of the resistant parent were recovered in most populations and one transgressive resistant line was found in Population 3. Transgressive segregates toward susceptibility were found in Populations 2, 3, and 4 for FHB. The heritability estimates were somewhat encouraging, as they indicated that moderate genetic gain can be expected when selecting for FHB resistance in a breeding program. However, a strong message was conveyed in the variable response of the parents and the ever present G x E interaction that FHB resistance breeding represents an unusually large challenge.
Abbreviations: FHB, Fusarium head blight • DON, deoxynivalenol • QTL, quantitative trait locus (loci)
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INTRODUCTION
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FUSARIUM HEAD BLIGHT has become the most devastating and economically important disease of malting barley and wheat (Triticum aestivum L.) in the U.S. upper Midwest. FHB of barley, also called scab and pink mold, is caused by the same fungus that causes seedling blight and root rot on small grains, and stalk rot of corn (Zea mays L.). The mycotoxin deoxynivalenol (DON) produced by this organism can make a potentially profitable barley crop unusable for malting, and substantially reduce its value as a feed grain. High levels of DON in barley are of concern to the malting and brewing industry, and some have zero tolerance for the presence of DON in the grain. Beer made from scabby barley can result in excessive foaming ("gushing"). Mycotoxins can be introduced into beer if present in barley used for malting, or if present in a brewing adjunct such as corn (Haikara, 1980; Schwarz et al., 1996). Scabby barley is toxic to humans and many animals, particularly swine, causing hyperestrogenism, excessive vomiting, or both (Mathre, 1982).
Most small grain cultivars are susceptible to FHB, and there is a lack of information about the genetic and environmental components influencing infection and disease development (Mesterházy, 1989). The first observation of differences in FHB susceptibility between wheat genotypes was made by Arthur (1891), who stressed the importance of breeding small grains for resistance. No immunity to FHB has been indentified in barley or other small grains. Most genotypes are susceptible, and current sources provide only partial resistance.
Investigation of the genetics of resistance to FHB in barley has not been very extensive and published reports on identification of loci controlling FHB resistance and DON accumulation are limited (Rudd et al., 2001). Takeda and Heta (1989) found large genotypic differences in FHB resistance among 5000 barley genotypes. Takeda (1990)(1993) found that resistance to FHB in the F2, F3, and F4 generations had a continuous distribution, suggesting that it is controlled by minor genes. In all populations and generations examined, two-row genotypes were the most resistant, followed by heterozygotes and then six-row genotypes. Heritabilities calculated on the basis of selection experiments (realized heritability) on five populations were 0.21 to 0.32 in the F2 to F3 generations, and 0.32 in plants pooled from these populations in the F3 to F4 generations (Takeda, 1990). Heritabilities estimated in the same populations by parent–offspring correlation were 0.46 on the F3 plant basis and 0.51 on the F3 line basis. Using the components of variance method and 282 barleys cultivars, Takeda et al. (1992) reported a heritability of 0.44. Gene action was found to be predominantly additive in an experiment involving an 8 by 8 and a 6 by 6 diallel cross with reciprocals (Takeda, 1993).
The objective of this research was to estimate the heritability of resistance to FHB resistance in progenies derived from four populations generated with four different sources of resistance.
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MATERIALS AND METHODS
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Parental Germplasm
Inheritance of resistance to FHB was investigated in four populations derived from crosses between resistant genotypes and five Midwestern U.S. elite lines or cultivars susceptible to FHB (Table 1). ‘Chevron’ (CI1111) was introduced to the USA from Switzerland (Shands, 1939), and has been the most widely used six-row source for resistance to kernel discoloration and FHB (Miles et al. 1989; de la Peña et al. 1999). ‘Gobernadora’, a two-row barley, was identified as a resistant line in China in 1987 in germplasm sent from ICARDA/CIMMYT (Mexico). It was released with the name of ‘Zhenmai-1’ in China (Vivar, 1997). GD2-27 is a six-row line derived from the cross of ‘Harrington’ x ‘Excel’ in the barley breeding program of the University of Minnesota. Zhedar 1 is a two-row introduction from China. The susceptible parents are cultivars or elite lines developed at the University of Minnesota (‘Stander’, Excel, ‘M69’, ‘M79’) and North Dakota State University (‘Foster’) breeding programs.
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Table 1. Pedigree of resistant and susceptible parents used in the study of the inheritance of resistance to FHB in barley.
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Populations
Data were obtained on lines derived from Chevron/M69, Gobernadora/Excel, GD2-27/M79, and Zhedar 1/Stander//Foster, designated Populations 1, 2, 3, and 4, respectively. Populations were grown at Crookston in 1995; St. Paul, Crookston, and Morris in 1996 and 1997; and also at Hangzhou, China, in 1997. Population 1 was at a F5:7 generation in 1995, Populations 2 and 3 were at F4:6 in 1996 and Population 4 was at F3:6 in 1996 and were advanced in bulk after the year the study started. A minimum of 40 six-row lines were selected from each population for study. The two-row lines obtained in the populations derived from crosses between two- and six-row parents (i.e., Populations 2 and 4) were not used in the study. The rationale was that 40 lines would be adequate to assess the magnitude of genetic diversity and G x E interaction. Population 1 was the most extensively tested; 101 lines over a span of 3 yr. This population also was utilized in molecular mapping research (de la Peña et al., 1999).
Disease Nurseries
Evaluation nurseries were grown at three locations in Minnesota from 1995 to 1997 (St. Paul, Morris, and Crookston), and also at Hangzhou, China, in 1997. Plot type and replication was similar in all nurseries. The genotypes were tested in one-row plots, 1.8 to 2.4 m long, with plots spaced 0.3 m apart in a randomized complete block design with two replications. To ensure that abundant inoculum and humidity were available to facilitate disease development, all nurseries were artificially inoculated and sprinkle or mist irrigated, except for the Crookston 1995 nursery, which was naturally infected with FHB (noninoculated).
Two types of FHB inoculum were applied in the different nurseries: mungbean broth with F. graminearum macroconidia and hyphal fragments (
1.8 x 106 propagules mL-1), and wheat, corn, or barley colonized kernels. The St. Paul nurseries were inoculated by applying 30 mL per plot of the mungbean broth, 2 to 3 times a week from anthesis to physiological maturity. The Crookston and Morris nurseries in 1996 were inoculated by spreading F. graminearum colonized wheat kernels over the plots 2 wk before anthesis (20 g plot-1). The inoculum was prepared with 12 different isolates collected in the Red River Valley of Minnesota the previous year. In 1997 the Crookston and Morris nurseries were inoculated by spreading colonized corn kernels over the plots, 2 wk before anthesis (10 g plot-1). The Hangzhou nursery in 1997 was inoculated by spreading F. graminearum colonized grains over the plots (5 g plot-1) at weekly intervals, for four consecutive weeks.
Moisture was applied in the nurseries with two different systems: St. Paul had a sprinkler irrigation system, whereas Crookston and Morris had a misting system. Sprinkler irrigation was applied each rain-free evening, from anthesis to physiological maturity, in the nurseries at St. Paul. Misting was initiated 2 wk before anthesis at Crookston in 1996. The plots were misted 10 min h-1, 24 h d-1, for 30 d. A total volume of 10.2 mm d-1 of water was applied. Because the disease reached excessive levels in some experiments in 1996, application frequency at Crookston in 1997 was reduced to 15 min h-1 for a 10-h period, every rain-free day. A total volume of 2.3 mm of water was applied every evening. Humidity was maintained at high levels by misting in the nursery at Hangzhou in 1997.
Disease Assessments
The FHB symptoms appeared as dark to brown stains on the palea and lemma of the kernel in the head and severity was usually assessed 18 to 21 d after anthesis by estimating the percentage of infected kernels from 20 heads per plot. The scale had eight percentage classes: 0, 5, 10, 15, 25, 50, 75, and 100%. In an average sized six-row head with 60 kernels, every three infected kernels represented 5% severity.
Heritability Estimates
Analysis of variance was first computed for FHB severity in each experiment, followed by a combined ANOVA of the experiments that presented significant genotypic differences (P 
0.10) for the trait. Data were included in the analysis only when there were observed statistically significant differences in the mean response of the lines present in the nursery. There were differences in the degree of FHB attributable to replications, environments and G x E interaction, and sometimes these factors seriously hampered the effort to identify differences among lines and in determining levels of resistance. In Population 1, significant genotypic differences among lines were obtained at Crookston in 1995 and 1996 and at Crookston, St. Paul, and Hangzhou in 1997. In Population 2, significant differences were found at Crookston and Morris in 1996 and at Crookston and Hangzhou in 1997. In the Population 3, data from Crookston and Morris in 1996 and Crookston in 1997 were used. In Population 4, data from Crookston and Morris in 1996 and at St. Paul and Morris in 1997 were used in the analysis. Frequency distributions of the disease scores from the populations were plotted using 0.25 of the mean standard deviation to establish class limits (Steel and Torrie, 1980; Conner, 1971, p. 363–367). Heritability estimates were calculated on an entry-mean basis from variance components. Heritability for each environment, considered as a location–year combination, was estimated from the variances obtained in a simple ANOVA (Table 2). Heritability estimates across environments were also computed from the variances obtained in an ANOVA by combining environments (Table 3).
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Table 2. Analysis of variance to be used for computation of heritability estimates by means of variance components from one location.
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Table 3. Analysis of variance to be used for computation of heritability with variance components from several locations.
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RESULTS AND DISCUSSION
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Data were obtained from three to five environments for each population. Single location analysis of variance was performed, followed by a combined analysis of variance of environments in which significant differences among lines were found. The combined analysis indicated significant environmental and G x E effects, except for G x E in Population 3 (Table 4).
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Table 4. Combined analysis of variance using data from environments where genotypic differences were found for FHB in Populations 1, 2, 3, and 4.
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Populations
FHB severity varied significantly among the different environments. Severity in the four populations ranged from very low at St. Paul in 1997, to very high at Crookston in 1996, as can be seen in the FHB values for the parents, population means and the resistant check Chevron in the different environments (Table 5). This range of severity scores indicates that FHB severity is highly influenced by the environment.
The fact that FHB development and expression is highly dependent on environmental conditions made it difficult to obtain useful disease data. Challenges were identified from the initial stages of this research. In one population not mentioned above (Zaoshu3/Excel), the level of resistance expressed in the parents differed for preliminary data but not for this research, causing the discard of this population. Even after some nurseries were discarded, parental scores and population means differed across environments, reflecting the importance that environment has on FHB severity. Chevron, which was used as a resistant check, sometimes appeared to be susceptible when severity in the nursery was very high.
Population distributions were nearly continuous in all crosses, with intermediate scores occurring most frequently, suggesting that FHB resistance is a quantitatively inherited trait (Fig. 1). There were breaks in the distributions that may be attributed to small populations that did not include all possible genotypes or could be explained in part by the scoring system, which failed to produce enough classes. In all populations, the resistant parents had lower severity scores than the susceptible parent. There were differences in resistance among the resistant parents, which had different pedigrees, that may be attributed to different numbers of genes conditioning resistance in the parents or to the influence of the genetic background. In Population 3, the severity scores of GD2-27 were numerically lower than for M79 in all environments, but the differences were not statistically significant (Table 5). In Population 4, Stander and Foster, the two susceptible parents in the three-way cross, did not differ in susceptibility (Table 5). In all populations, the resistant parent had the same resistance levels as the resistant check, Chevron, except in Population 3, where the level of resistance expressed by GD2-27 was well below that of the resistant check Chevron (Table 5).
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Fig. 1. Distribution of FHB scores for barley paremnts and lines in Population 1 (Chevron/M69), Population 2 (Gobernadora/Excel), Population 3 (GD2-27/M79), and Population 4 (Zhedar1/Stander//Foster). N = number of environment in which the populations were tested;  = population mean.
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In Populations 1 and 3, the most resistant lines had similar or lower scores than the resistant parent (Fig. 1). In Populations 2 and 4, no lines showed the same levels of resistance as the resistant parent and the most resistant lines had severity scores significantly higher than Gobernadora and Zhedar 1. The resistance levels of the resistant parent were not recovered in the 40 lines of these populations (Fig. 1). Population 4 was derived from a three-way cross with two susceptible parents, which would have markedly reduced the number of resistant lines. The discard of the two-row genotypes from the populations derived from crosses between a resistant two-row and a susceptible six-row parent (Populations 2 and 4) could also have skewed the distributions toward susceptibility. Some studies published after our research was initiated confirmed preliminary observations made by Takeda and Heta (1989), indicating that in general two-row genotypes are more resistant to FHB than six-row genotypes (Steffenson, 1996; Zhu et al., 1999). A relatively minor quantitative trait locus (QTL) conferring resistance to FHB coincident with a QTL determining head type has been found in some mapping studies (Zhu et al., 1999; Mesfin et al., 2003), thus higher level of susceptibility could be expected if only the six-row are evaluated in the populations. However, QTL providing resistance to FHB have been identified on all seven barley chromosomes (de la Peña et al., 1999; Ma et al., 2000), therefore the loss of a small resistance QTL linked or pleiotropic for head type should not sensibly increase the susceptibility levels in the six-row lines, given that the main resistance QTL were expected to still be segregating in the population lines. Transgressive segregation toward resistance was present only in Population 3 (Fig. 1). In Population 1, the most resistant lines had severity scores lower than Chevron, but they did not differ significantly from Chevron in the over-all analysis. The severity scores of the most resistant lines were relatively inconsistent from environment to environment (data not shown). The inherent variability associated with this disease made it difficult to determine whether the genotypes with lower scores had resistance superior to Chevron or had low scores due to nongenetic variation. The population mean was numerically lower than the midparent value only in Population 1, indicating slightly greater resistance than expected from the parental performance (Table 5).
In Populations 2, 3, and 4, the most susceptible lines had severity scores higher than the susceptible parents and some lines were significantly more susceptible. This was most apparent in Population 2, in which almost all lines in the population had higher severity values than Excel, the susceptible parent (Fig. 1). In Populations 2 and 4 the overall population mean was well above the mid-parent value (Table 5), indicating higher levels of susceptibility than expected from parental performance.
Susceptibility near or even higher than the level of the susceptible parents was relatively common. Transgressive segregation toward susceptibility was observed in all Populations except in Population 1 (Fig. 1). The most likely explanation is that both parents in those crosses possess genes that contribute to susceptibility or by the breakup of epistatic gene combinations. A quantitatively inherited disease that exhibited transgressive segregation and skew toward susceptibility has been also reported in studies of resistance to kernel discoloration in barley (Miles et al., 1987, 1989).
Heritability Estimates
The estimates of heritability for FHB based on line-means for the individual environments differed among crosses, including low, intermediate and high values (Table 6). Population 1 heritability ranged from low at Crookston in 1996 to relatively high at the same location in the following year (Table 6). For Population 2 the heritability estimates ranged from intermediate for Crookston in 1996 to high for Morris in the same year. Population 3 had the lowest estimates in each environment. In general, the values support the proposition that genetic differences in FHB reaction are moderately heritable. However, the several environments that were omitted from analysis indicated that finding moderate heritabilities depends on having appropriate FHB levels in the nursery.
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Table 6. Heritability estimates obtained by components of variance (line-mean basis) of FHB in Populations 1, 2, 3, and 4 in all the environments tested .
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Estimates of heritability tended to be highest when data were collected in nurseries with intermediate infection levels, as at Crookston 1997 for Population 1 or Morris 1996 for Populations 2, 3, and 4. They tended to be lower in nurseries with low and especially high disease levels (Tables 5 and 6). We hypothesize that low levels of FHB lead to escapes which influence genetic differences and genotype x replication interaction and that very high disease levels tend to overcome resistance even in the most resistant parents and lines.
Heritability estimates for FHB for the four populations on the basis of three to five environments ranged from intermediate to relatively high. Population 1 and 4 had the lowest heritability. Heritability was high for Population 3 (Table 6). Since these estimates take G x E interaction into account they are assumed to be a relatively reliable estimate of genetic versus environmental effects in segregating populations and are better predictors of genetic gain than the single environment estimates. They indicate that gains equal to about one-half of the selection differential can be expected.
It is anticipated that heritability will be highest in the crosses where parents show the largest severity differences. However, in Population 3, where the parents had intermediate and similar resistance levels, considerable genetic variance was found and the heritability estimates were similar to those found in Populations 1, 2, and 4 where parent differences were sizeable. Apparently, both parents in Population 3, GD2-27 and M79, had genes which conditioned an intermediate severity reaction indicating that their array of resistance alleles was different.
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CONCLUSIONS
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Data support the hypothesis that genotypes with higher FHB resistance than either parent can be selected from populations derived from crosses between parents that show intermediate levels of resistance or even susceptibility. Combining FHB resistance genes from different sources to produce transgressive segregants with higher levels of resistance has been proved to be possible, although it seems that transgressive segregation toward susceptibility is easier to obtain than toward resistance. Often the resistance of the parents is not enough to protect adequately against severe FHB epidemics, and there is the empirical question of how useful or acceptable are the levels of resistance achieved in the offspring, even if they are higher than in the parents. Following a recurrent-type selection strategy would allow the accumulation of resistance genes from diverse sources, which could increase the chance to reach enhanced levels of resistance.
The experience acquired in this research indicates that designing screening nurseries to reach the desired disease levels is as important as the selection of the correct resistance sources and breeding strategies for the success of the breeding program. While the findings are somewhat encouraging from the standpoint of making genetic gain from selection for FHB, there was a strong message that because of the quantitative nature of the resistance, the environmental influence mentioned everywhere above, and the costs of setting up a correct screening system, FHB resistance breeding represents an unusually large challenge.
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ACKNOWLEDGMENTS
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The authors acknowledge funding from grants from the American Malting Association for supporting this research. We also would like to thank the North Dakota State University Barley Breeding Program and Dr. Richard Horsley for supplying Population 4. We are grateful to Dr. Jose Crossa for reviewing the manuscript.
Received for publication July 9, 2002.
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ABSTRACT
INTRODUCTION
