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CROP BREEDING, GENETICS & CYTOLOGY

Inheritance of High Levels of Adult-Plant Resistance to Stripe Rust in Five Spring Wheat Genotypes

^a Department of Agricultural, Food, and Nutritional Science, 410 Agriculture/Forestry Center, University of Alberta, Edmonton, AB, Canada, T6G 2P5
^b CIMMYT, Apdo, 6-641, 06600 Mexico, DF, Mexico

^* Corresponding author (JP.Tewari{at}ualberta.ca).

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Inheritance of adult-plant resistance to stripe rust (caused by Puccinia striiformis Westend. f. sp. tritici) in five spring wheats (Triticum aestivum L. em. Thell) following inoculation with the Mexican race Mex96-11 was studied. All possible crosses among these resistant genotypes and a susceptible genotype, ‘Avocet-YrA’, were made in a one-way diallel mating design. F₁ crosses, F₂ populations, and F₂:F₃ and F₅ single seed-descent lines were evaluated under artificial field epidemics initiated with race Mex96-11. The adult-plant resistance in crosses of resistant parent with Avocet-YrA tended to be incompletely dominant and was based on the interaction of gene Yr18 and at least three additional additive genes in each parent. Transgressive segregation was detected in all F₂ populations and F₅ single seed-descent lines of the resistant parent inter-crosses, indicating that some additive genes were nonallelic. Combining ability analyses indicated that additive gene effects were more important than nonadditive gene effects in the inheritance of adult plant resistance to stripe rust in the evaluated material. Estimates of narrow-sense heritability ranged from 0.88 to 0.96. Stripe rust resistance in these wheats is expected to be durable.

Abbreviations: APR, adult-plant resistance • GCA, general combining ability • HPTR, homozygous for the parental type resistance • HPTS, homozygous for the parental type susceptibility • PTR, parental type resistant • PTS, parental type susceptible • SCA, specific combining ability • SegI, segregating intermediate • SegS, segregating susceptible • SSD, single seed-descent

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
STRIPE RUST is an important fungal disease of wheat in many countries (Roelfs et al., 1992). Genetic resistance is the most effective, economical, and environment-friendly method of managing stripe rust. More than 30 genes that confer resistance to stripe rust in wheat have been cataloged (McIntosh et al., 1998). A majority of these resistance genes are expressed in the seedling growth stage, are effective throughout the life of the plant, and are characterized by a hypersensitive response. However, high genetic variation and the ability of the pathogen to evolve into new races with added new virulence always have been the major limiting factors in a successful long-term management of stripe rust when race-specific resistance genes are used. "Breakdown" of such race-specific stripe rust resistance genes as a consequence of pathogen acquiring new virulence has frequently been reported, even in cases where race-specific resistance genes are used in combination (Johnson, 1988). Adult-plant resistance (APR) in spring and winter wheat genotypes is a type of interaction between the host and pathogen, in which the adult plant is partially resistant, despite seedling compatibility (Bariana et al., 2001; Zhang et al., 2001; Wagoire et al., 1998; Bariana and McIntosh, 1995; Singh and Rajaram, 1994; Chen and Line, 1995b; Milus and Line, 1986; Johnson, 1980). McIntosh (1992) indicated that durable rust resistance is more likely to be of the adult-plant, rather than seedling type, often conditioned additively by more than a single gene, and is not associated with genes conferring hypersensitive response. Stripe rust resistance gene Yr18, located in chromosome arm 7DS (McIntosh et al., 1998) is a major contributor to durable APR to stripe rust. Under high disease pressures, however, stripe rust severity of lines with Yr18 alone often reaches 50 to 60% (Ma and Singh, 1996), which is not acceptable in breeding programs. Incorporating additional resistance genes to Yr18 may result in greater resistance (Singh et al., 2000).

The parental genotypes studied derive from a breeding project at the International Wheat and Maize Improvement Center (CIMMYT), designed to combine Yr18 with other additive APR genes to achieve improved APR in high-yielding wheat germplasm. These attempts resulted in lines with APR that were phenotypically indistinguishable from lines with hypersensitive genes (Singh et al., 2000). The objectives of the present study were to determine the number of effective genes and to study the combining abilities and gene effects for APR to stripe rust in a one-way diallel cross involving five APR spring wheat genotypes and a susceptible spring wheat genotype, Avocet-YrA.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Five spring wheat genotypes were chosen for a genetic study on the basis of their APR to stripe rust at several locations, despite their high infection type response in the seedling growth stage to the Mexican race, Mex96-11 (Table 1). Mex96-11 is the predominant race in the highlands of central Mexico where field experiments were performed. One-way diallel crosses were made among the five resistant genotypes and a susceptible Australian cultivar, Avocet-YrA, in the greenhouse at the University of Alberta, Edmonton, Canada. From each cross, 90 to 150 F₁ seeds were harvested. Ten F₁ seeds from each of the 15 crosses were grown in a greenhouse and were self-pollinated to produce F₂ seeds that were harvested from individual plants in each cross. The F₂:F₃ lines of the susceptible x resistant crosses were obtained from F₂ single plants. The F₂ to F₄ generations of all 15 crosses were advanced by single seed-descent (SSD) in the greenhouse. The F₅ SSD lines were obtained by harvesting single F₄ plants, which were space-planted at the University of Alberta Edmonton Research Station in the summer of 2000.

Field evaluations were performed at the CIMMYT Research Station near Toluca (State of Mexico) in the highlands of central Mexico (19°N, 2640 meters above sea level), during the 2000 and 2001 crop seasons. The Toluca Station has a favorable environment for stripe rust development. Parental lines, F₁ crosses, F₂ populations, and F₂:F₃ lines were evaluated in 2000. The F₁ and F₂ diallel experiments consisted of 15 F₁s or F₂s derived from the diallel cross and six parental lines. Each experiment was planted in a randomized complete block design with three replicates. The F₁ experimental units comprised of 15 plants and were grown in 1 m plots in 75 cm wide raised beds in two rows, 20 cm apart, while F₂ experimental units were comprised of 120 space-sown plants at 10- to 15-cm spacing in 75 cm wide beds 2.5 m long. About 80 seeds of each of the 624 F₃ lines, 118 to 130 from each susceptible x resistant cross, were planted in a plot of the same size as for the F₁ experiment, with parental lines repeated after every 10 lines as checks.

The six parents, 564 F₃ lines derived from the five susceptible x resistant crosses, 68 to 155 lines from each cross, 1810 F₅ lines derived from all 15 crosses, and 75 to 142 lines from each cross were included in the 2001 trial. Lines were planted in an augmented randomized complete block design (ARCBD) as described by Scott and Milliken (1993). Each block consisted of 200 experimental units. One set of 10 check genotypes with different stripe rust responses was randomly planted in each block. Plot size and seed density was the same as described for the F₃ experiment in 2000.

In all field experiments, one row of the susceptible spreader cultivar, Morocco, was planted on one side of the plots in the pathways and around the experiments. Artificial inoculation was done with a single race of P. striiformis f. sp. tritici, MEX96-11, virulent on Yr 2, (3), 6, 7, 9, 27, and A, 4 wk after sowing. For this purpose, fresh urediniospores suspended in a lightweight mineral oil (Soltrol-170; Houghton Chemical Corporation, Allston, MA) were sprayed on the spreader rows. The parental genotypes were tested earlier for seedling reaction to race MEX-96-11 at CIMMYT (Table 1) and all displayed a high infection type (8–9 in a 0-to-9 scale; McNeal et al., 1971). Therefore, this race was suitable for the study of APR.

Stripe rust severity of the F₁ crosses, F₂ single plants, and F₃ and F₅ lines were rated following the modified Cobb's Scale (Peterson et al., 1948). This visual scale is used to estimate the percentage of tissue rusted. The disease severity is considered to be 100% if 37% or more of the leaf area is affected (Roelfs et al., 1992). Plants of lines were evaluated for disease reaction at two separate times (Singh and Rajaram, 1994). The plots were evaluated first when the susceptible parent, Avocet-YrA, showed 80 to 100% severity. Two weeks later the plots were evaluated again when rust had desiccated the leaves of Avocet-YrA. Disease severity in F₁, F₃, and F₅ experiments were assessed on the basis of the average rust severity on the flag and penultimate leaves in the plots. An overall disease severity was visually estimated for each plot. In the F₂ experiment, however, all single plants in each experimental unit were evaluated for rust severity. Several flag and penultimate leaves of each single plant were evaluated and an average rust severity was estimated for each plant.

For segregation analysis, single plants in each F₂ population derived from susceptible x resistant crosses were classified into three groups: (i) parental type resistant (PTR)—those with disease severities equal or less than that of the resistant parent; ii) parental type susceptible (PTS)—those with disease severities equal or greater than that of the susceptible parent; and (iii) others. In F₃ and F₅ of the susceptible x resistant crosses, lines were classified into four groups: (i) homozygous for the parental type resistance (HPTR); (ii) homozygous for the parental type susceptibility (HPTS); (iii) segregating or homozygous for disease severity levels greater than that of the resistant parent but less than that of the susceptible parent (SegI); and (iv) segregating with at least one plant having disease severity similar to the susceptible parent's response (SegS). The distribution of observed phenotypic frequencies was tested against expected segregation models by a Chi-square test. Frequency distributions of the disease severity of F₂ plants and F₅ lines of the resistant parent intercrosses were used to study the similarity of segregating factors.

Quantitative genetic analysis of the diallel cross used the plot mean values of the disease severities for F₁ crosses, F₂ populations, and F₅ lines. The treatment residuals were not normally distributed as determined by the Shapiro-Wilk statistic (Shapiro and Wilk, 1965) computed by the PROC UNIVARIATE procedure (SAS Institute, 1990). Percent mean disease severity of each experimental unit therefore was transformed by the arcsine of the square root to normalize the scale. To test the null hypothesis of no genotypic differences among the treatments (parents, F₁ crosses, and F₂ populations), a one-way analysis of variance (Steel et al., 1997) was performed (PROC GLM, SAS Institute, 1990). Treatment sum of squares were broken into three components, parents (P), crosses (C), and P vs. C. The F₃ and F₅ lines in augmented designs were analyzed separately by the PROC GLM and PROC MIXED procedures (SAS Institute, 1990) as described by Scott and Milliken (1993) with minor modifications. This estimated the main effect of treatment and the nested effect of lines within treatment and partitioned the treatment sum of squares into four main components, parents (P), crosses (C), checks, and P vs. C.

Combining ability analyses were conducted separately for F₁, F₂, and F₅ diallel following Model I, Method IV of Griffing (1956), with treatment considered as fixed. Diallel Analysis and Simulation Software by Burrow and Coors (1994) was used to estimate the general combining ability (GCA) and specific combining ability (SCA) effects and the components of variance. The model used in the combining ability analysis of F₁ and F₂ was:

where X_ijk = observed average value of the experimental unit for F₁ and F₂, µ = population mean, g_i = GCA effect for parent i, g_j = GCA effect for parent j, s_ij = SCA for parents i and j, b_k = rep (block) effect for block k, and e_ijk = error. The model assumes that epistasis and genotype x environment interaction effects are not significant. Parents were not included in the combining ability analysis to obtain unbiased estimates of GCA and SCA parameters (Das and Griffey, 1994; Singh et al., 1992). For the F₅ diallel, the GCA and SCA effects were estimated on the basis of the mean stripe rust severities of the F₅ SSD lines within each cross and were tested by the mean square of the nested effect of lines within treatments in the ANOVA. The ratio 2²_g/ was computed (Baker, 1978) to estimate the relative importance of GCA and SCA. Narrow-sense heritability of the disease severity was estimated for each generation from the estimated components of variance, as the ratio of additive variance to the sum of genotypic and environmental variance. Mean stripe rust severities of F₁ crosses and F₂ populations, and least square mean of the severities of F₃ and F₅ lines were computed using MEANS and LSMEANS statements, respectively, in the PROC GLM procedure. The hypothesis of the similarity of the means in F₁ and F₂ diallels was tested by Tukey's standardized range test (SAS institute, 1990). Minimum number of additive APR genes in the resistant parents were estimated on the basis of the quantitative data in susceptible x resistant crosses in F₁, F₂, and F₅ generations according to the formulae proposed by Mather and Jinks (1982) and Bjarko and Line (1988). The formulae are based on the assumptions that segregating resistance genes derived from a single parent, are unlinked, and have equal additive effects. Also, dominance, additive x dominance–epistasis, and genotype x environment effects are assumed to be unimportant.

	RESULTS

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The mean terminal stripe rust severities of the parental genotypes, F₁ crosses, F₂ populations, and least square means of the F₃ and F₅ SSD lines, and 10 check-genotypes are presented in Table 2. Although the stripe rust severities of the resistant parental lines were slightly higher in the second year, all five of them displayed low levels (between about 1–10%) of stripe rust severity, which was less than the 100% severity of the susceptible parent, Avocet-YrA. ‘Simorgh’ was the most resistant parent in all experiments. The relative disease severity levels among the other APR parental genotypes and crosses varied slightly between years and trials with a high correlation [r = 0.95 (P < 0.01) to r = 0.99 (P < 0.01)] among parents and crosses for stripe rust severity.

View larger version (34K): [in this window] [in a new window]   Fig. 1. Relative frequency distribution of stripe rust severity of F2 population (top), F2–derived F3 lines (middle), and F5 SSD lines (bottom) derived from Avocet-YrA x Cocnoos cross, evaluated under artificial epidemics of race Mex96-11 in Toluca, MX (2000–2001).

Although none of the F₂ plants derived from the resistant parent intercrosses were as susceptible as Avocet-YrA, single F₂ plants with stripe rust severity levels higher than those of parental lines were observed in all F₂ populations (data not shown). Disease severity as high as 50% was observed in F₂ populations derived from ‘Saar’ x ‘Parastoo’ and Simorgh x Parastoo. The F₅ lines of the resistant-parent intercrosses also were evaluated to verify the F₂ results. The level of segregation for stripe rust severity varied among the F₅ populations of the resistant x resistant crosses. The populations derived from crosses Saar x ‘Homa’ (² = 210.2 ± 1.2) and Saar x Parastoo (² = 174.2 ± 1.1) had higher variance with three and five lines reaching disease severities as high as 60%, respectively. Saar x Simorgh (² = 82.8 ± 0.7) and Simorgh x Homa (² = 65.6 ± 0.7) had lower variance with only one line reaching 40% severity in each population. This indicated that although all resistant parents probably have at least one gene in common, some of the other additive genes in each of the parents are different. If we consider that on the average each parent had two genes in common for stripe rust resistance and they differed by two additive genes, then a total of twelve different additive genes might be present in the parents.

Differences in variances were highly significant (P < 0.01) for parents, F₁ crosses, F₂, F₃, and F₅ populations (Table 4). From the F₃ lines, only susceptible x resistant derivatives were evaluated. The parent vs. F₁ cross effect was significant (P < 0.05), and parent vs. F₂ population and parent vs. F₃ lines effects were highly significant (P < 0.01). The F₁ crosses, and F₂ and F₃ population means deviated from their mid-parental values. This effect was not significant for the F₅ lines. Reduced dominance effects in the F₅ due to a high degree of homozygosity of lines likely resulted in the alignment of population means and mid-parent means. General combining ability effects were observed for F₁, and F₂ (P < 0.01), and for F₅ (P < 0.05) populations, while SCA effects were observed only in F₁ (P < 0.05) and F₂ (P < 0.01) experiments (Table 4). The components of variance ratios were 0.95, 0.97, and 0.93 for F₁, F₂, and F₅, respectively, and therefore GCA was more important than SCA in predicting the progeny performance. The importance of GCA also was evident based on the high correlations between parental means and GCA effects (r = 0.95, P < 0.01, for F₁; r = 0.97, P < 0.01, for F₂; and r = 0.97, P < 0.01, for F₅). Narrow-sense heritability estimates were also relatively high being 0.91, 0.96, and 0.88 for F₁ crosses, F₂ populations, and F₅ SSD lines, respectively.

Specific combining ability effects were significant in the F₁ (P < 0.05) and F₂ (P < 0.01) generations, but not in the F₅ generation (Table 4). In crosses with the susceptible parent, the cross Simorgh x Avocet-YrA had the greatest negative SCA in the F₁ (SCA effect = –17.85; P < 0.01) and in the F₂ (SCA effect = –4.79; P < 0.01) generations (Table 5). This indicated that Simorgh contributed the greatest reduction in disease severity when crossed with the susceptible parent. In resistant parent intercrosses, the cross Saar x Cocnoos had negative SCA effects across all three generations (SCA effect = –5.76; P < 0.05 for F₁, –3.51; P < 0.01 for F₂, and –4.06; P < 0.01 for F₅).

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Comparison of stripe rust severities of the five resistant parents with their respective F₁ in crosses with the susceptible parent and the midparental values in susceptible x resistant crosses indicated that APR to stripe rust tends to be incompletely dominant. Segregation results indicated that the APR to stripe rust in these resistant parents was controlled by a minimum of four genes with additive effects. All resistant parents carried the leaf tip necrosis gene that is known to be either pleiotropic or linked to Yr18 (Singh, 1992). Therefore, Yr18 gene was one of the genes identified in each parent. The skewness of the frequency distributions of the F₅ lines and the shift of F₁ values and F₂ and F₃ population means from the mid-parental values toward the resistant parent in susceptible x resistant crosses was probably due to the greater effect of Yr18 than other genes.

Additive gene effects were major contributors to the inheritance of stripe rust severity. The preponderance of GCA effects, as was demonstrated by the components of variance ratio, showed that the additive gene effects were more important than non-additive gene effects in the evaluated genotypes. The estimates of narrow-sense heritabilities were also relatively high and were in agreement with the importance of additive gene effects. Our results are consistent with those of Ghannadha et al. (1995), Krupinsky and Sharp (1978), and Wagoire et al. (1998), who reported the importance of additive gene effects in the inheritance of latent period, infection type, and coefficient of infection to stripe rust.

The relative importance of additive over nonadditive gene effects suggested that the most resistant progeny might be derived from crosses with genotypes with greatest negative GCA. The GCA and SCA effects were slightly inconsistent across the generations. Das and Griffey (1994) stated that the inconsistency of GCA effects across generations could have resulted from segregation and recombination of resistance genes. Combining ability of more advanced generations, therefore, seems to be more reliable. Simorgh was the most resistant parent in all experiments with the greatest negative GCA in the F₅ generation. Cocnoos also had a high negative GCA effect and can be considered as a good general combiner for APR to stripe rust.

Parent vs. crosses effects indicated the existence of deviation of F₁ and F₂ means from mid-parent values due to the presence of non-additive gene effects. This effect was not observed in the F₅ generation, probably because of the reduced dominance variance resulting from increased homozygosity. Additionally, the significance of SCA effects in F₁ and F₂ indicate the presence of nonadditive gene effects. Wagoire et al. (1998) reported the presence of significant dominance and epistatic gene effects, while the additive gene effect was the major component in the inheritance of coefficient of infection to stripe rust. Chen and Line (1995a) also reported the presence of significant dominance and epistatic gene effects in the inheritance of high-temperature adult-plant resistance in ‘Druchamp’ wheat. However, Vanderplank (1984) cautioned that quantitative genetic analysis of disease resistance often is associated with an overestimate of nonadditive and an underestimate of additive gene effects. The nonadditive gene effect estimated in this research might be, at least in part, due to overestimation of the nonadditive gene effects because of the visual scale which was used for disease assessment.

Although all resistant parents carry the Yr18 gene, stripe rust severities among the F₂ and F₅ derivatives reached 50 to 60% in some plants of resistant parent intercrosses. Therefore, some of the additive genes in each resistant parent are different. Those with 50 to 60% stripe rust severity in resistant parent intercrosses were probably the plants or lines with Yr18 alone. This is in accordance with the known moderate effect of Yr18 gene under high disease pressure when present alone (Ma and Singh, 1996). In such crosses, it is likely that only Yr18 is the common gene and other genes are different, suggesting the possibility of combining these genes to achieve lines with more additive APR genes in a genetic background.

Our results demonstrated that high levels of APR to stripe rust could be achieved by combining a few additive genes. This is in agreement with the findings of Wallwork and Johnson (1984), Bariana and McIntosh (1995), Singh et al. (2000), Singh and Rajaram (1994), and Bariana et al. (2001), who reported involvement of a few additive genes in inheritance of different levels of APR. Even in the case of lines with high levels of APR, variation does exist for additive resistance genes and pyramiding APR genes by intercrossing APR lines is feasible. Such transgressive lines may be needed for areas where stripe rust is severe.

	ACKNOWLEDGMENTS

 
The PhD fellowship of the first author was supported through funds provided to CIMMYT by the Agricultural Research and Education Organization of the Ministry of Agriculture Iran. The research costs in Mexico were supported by CIMMYT, whereas, those in Canada were supported through a matching grant from the Alberta Agricultural Research Institute.

Received for publication February 11, 2003.

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