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Published online 7 November 2007
Published in Crop Sci 47:2303-2307 (2007)
© 2007 Crop Science Society of America
677 S. Segoe Rd., Madison, WI 53711 USA
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CROP BREEDING & GENETICS

Heritability Estimates and Response to Selection for Resistance to Mycosphaerella Blight in Pea

Roger X. Zhanga and Bruce D. Gossenb,*

a Alberta Research Council, Vegreville, AB T9C 1T4, Canada
b Agriculture and Agri-Food Canada, Saskatoon, SK S7N 0X2, Canada

* Corresponding author (gossenb{at}agr.gc.ca).


   ABSTRACT
TOP
 NOTES
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Resistance to Mycosphaerella pinodes in field pea (Pisum sativum L) is a quantitative trait, and expression of resistance is substantially influenced by environment. The disease reaction to mycosphaerella blight of four crosses (F2:4 and F2:5 populations) was assessed in field trials at Vegreville, AB, Canada. Broad-sense heritability of resistance was quite high (0.62–0.81). Narrow-sense (realized) heritability was moderate (0.43–0.57), indicating that additive genetic factors contributed substantially to the resistance phenotype. Significant improvement in resistance among the lines developed from selected individuals indicates that genetic improvement based on progeny testing would be effective. This study demonstrated that resistance to M. pinodes can be improved through progeny selection from crosses of the most resistant lines.

Heritability Estimates and Response to Selection for Resistance to Mycosphaerella Blight in Pea

Roger X. Zhanga and Bruce D. Gossenb,*

a Alberta Research Council, Vegreville, AB T9C 1T4, Canada
b Agriculture and Agri-Food Canada, Saskatoon, SK S7N 0X2, Canada

* Corresponding author (gossenb{at}agr.gc.ca).

Resistance to Mycosphaerella pinodes in field pea (Pisum sativum L) is a quantitative trait, and expression of resistance is substantially influenced by environment. The disease reaction to mycosphaerella blight of four crosses (F2:4 and F2:5 populations) was assessed in field trials at Vegreville, AB, Canada. Broad-sense heritability of resistance was quite high (0.62–0.81). Narrow-sense (realized) heritability was moderate (0.43–0.57), indicating that additive genetic factors contributed substantially to the resistance phenotype. Significant improvement in resistance among the lines developed from selected individuals indicates that genetic improvement based on progeny testing would be effective. This study demonstrated that resistance to M. pinodes can be improved through progeny selection from crosses of the most resistant lines.


   INTRODUCTION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 CONCLUSIONS
 REFERENCES
 
MYCOSPHAERELLA BLIGHT, caused by Mycosphaerella pinodes (Berk. and Blox.) Vesterg. (anamorph: Ascochyta pinodes L.K. Jones), is a major disease problem of field pea (Pisum sativum L.) worldwide (Xue et al., 1998; Onfroy et al., 1999; Gurung et al., 2002; Pretorius et al., 2002). Inherence of resistance to M. pinodes is a quantitative trait controlled by multiple genes (Prioul et al., 2004; Loridon et al., 2005; Zhang et al., 2006, 2007; Prioul-Gervais et al., 2007). Differences in susceptibility have been demonstrated among cultivars (Zhang et al., 2006), but no strong sources of resistance are known in P. sativum. As a result, sources of resistance are being sought in wild species of P. sativum (Wroth, 1998) and closely related species like Lathyrus sativus (Skiba et al., 2004).

Estimates of heritability measure the heritable variation between genotype and phenotype (Henninger et al., 2000). Broad-sense heritability measures how frequently a trait is expressed (Dudley and Moll, 1969) and is typically defined as the ratio of the genotypic variance ({sigma}2G) to the phenotypic variance ({sigma}2P) of individuals in the population (Nyquist, 1991). Realized heritability (narrow-sense heritability) is the additive genetic component estimated from response to selection (Lynch and Walsh, 1998) and is defined as the ratio of the observed response to the total response possible (Hedrick, 2000). Response to selection (R), calculated from selection differential and realized heritability, is an estimate of how much the selected progeny differ from the parental population (Scharloo, 1991).

The objectives of this study were to confirm the inheritance of resistance to M. pinodes and to estimate the narrow-sense heritability of resistance. These factors are important for improving resistance to M. pinodes (Wroth, 1999). This represents the first report of estimates of realized heritability and selection response of resistance to M. pinodes from a breeding program.


   MATERIALS AND METHODS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS AND DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Plant Materials and Field Design
Parental lines were selected to represent the range of disease reaction available in commercial cultivars and breeding lines, from highly susceptible to moderately susceptible (Table 1 ), based on a previous study (Hwang et al., 2006). Four crosses (‘Tara’/JI 2480; PI 203069/PI 179449; ‘Radley’/Tara; CEB 1171/Radley) were selected to produce a wide range of potential interactions in the progeny. The crosses were made in 2003 in the field. The F1 plants were grown and allowed to self-pollinate in a greenhouse over the winter of 2003–2004. Subsequent generations were produced using single-seed descent in field trials from 2004 to 2006. Selections were conducted in F2:4 in 2005, and 28 to 39 of the most resistant individuals from each combination were selected to develop F4:5 families in 2006. Both F4:5 families and F2:5 populations were planted out in 2006.


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  		Table 1. Seed source and mycosphaerella blight reaction of Pisum sativum lines used as parents.

 
Field trials were conducted at the research farm of the Alberta Research Council, Vegreville, AB, Canada, in 2005 and 2006, in fields where P. sativum had never been grown. Each plot consisted of one row, 10 m in length, with 30 cm between plants within each row. Rows were spaced 90 cm apart. The plots of each cross were planted as a block with a single level of replication, arranged as follows: parental lines, F2:5 population, and F4:5 selected. Plots of the susceptible line PI 179449 and moderately susceptible cultivar Radley were planted with every cross as controls. The seed was hand-planted into moist soil in mid-May each year. Reaction to mycosphaerella blight was assessed in mid-August (late flowering) each year. Data collected from F2:4 selected and F2:4 population in 2005 and F4:5 families (derived from F2:4 selected) and F2:5 population in 2006 were used for analysis.

Inoculum preparation and application were as described previously (Zhang et al., 2007). Briefly, conidia were harvested from cultures of a highly aggressive single-spore isolate of M. pinodes from a field pea crop in Alberta that was grown on agar media for 4 wk at 20°/15°C (day/night) and 16-h photoperiod. The spore suspension was applied to an inoculum medium (10 peat moss:2 autoclaved soil:1 sand, w/w), which was distributed evenly in the plots at 1 x 107 spores m–2 at the early flowering stage (20–30 June). We inoculated these trials to guarantee uniform distribution of primary inoculum under conditions that were suitable for blight development. All of the individual plants of each population were rated once for mycosphaerella blight at late flowering in mid August, using a 0 to 9 scale (Xue et al., 1996), where increasing scores represent higher disease severity and disease development occurring higher in the plant canopy (0 = healthy plant, 9 = severe disease in the upper portion of the plant).

Data Analysis
Analysis of variance for each trial was performed using PROC GLM of SAS (SAS Institute, Cary, NC) and variance components were calculated using PROC VARCOMP. Restricted maximum likelihood estimates of the covariance components and correlation coefficients were obtained using PROC MIXED. Genotypic variance ({sigma}2G) and environmental variance ({sigma}2E) were estimated as

Formula 1[1]

Formula 2[2]
where {sigma}2F2:5 represents F2:5 population variance and {sigma}2P1 and {sigma}2P2 represent the variance of each parent (Lande, 1981).

Broad-sense heritability (H) was estimated from variance components as (Nyquist, 1991)

Formula 3[3]
Realized heritability (h2) was calculated as

Formula 4[4]
where Formula 4F4:5 selected is the mean blight severity rating of F4:5 families derived from selected F2:4 individuals; Formula 4F2:5 pop is the mean of F2:5 populations derived from F2:4 lines by single seed descent; Formula 4F2:4 selected is the mean of selected F2:4 individual plants; and Formula 4F2:4 pop is the mean of the F2:4 population (Hallauer and Miranda, 1988).

Response to selection (R) was calculated as

Formula 5[5]
where S represents the selection differential derived from the product of the selection intensity (i) x phenotypic deviation ({sigma}P), Covpo is the covariance of parents and offspring, and {sigma}2P is the phenotypic variance of the selection unit (parents) (Falconer and Mackay, 1996).

The covariance was calculated as

Formula 6[6]
where i and j are the variables of parents and offspring, respectively, and n is the sample size (Neter et al., 1990).

Correlations were calculated as

Formula 7[7]
where rg is the genetic correlation between evaluations in 2005 and 2006; i, variance A, and j, variance B; Cov(ij) representing the average additive genetic covariance between i and j; {sigma}2(i) is the average additive genetic variance for i; and {sigma}2(j) is the average additive genetic variance for j (Searle, 1961).


   RESULTS AND DISCUSSION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
CONCLUSIONS
 REFERENCES
 
The distribution of mycosphaerella blight reaction of individual plants in the populations from the four crosses and the parental lines are presented in Fig. 1 . Individual plants differed substantially in disease reaction, indicating that the largest source of variation was the contribution of the parent lines. A few individuals from each cross had levels of resistance that were slightly higher than the parents (Fig. 1). The pattern of variation among the four populations supports the conclusion of previous reports that inheritance of resistance to M. pinodes is quantitative (e.g., Zhang et al., 2006, 2007). The genetic mechanisms that control resistance to M. pinodes have been shown to differ among lines (Timmerman-Vaughan et al., 2002). This indicates that different resistance genes occur in various populations (Salgado et al., 1995). The correlation of F2:4 and F2:5 was significant (P < 0.001) for each cross (Table 2 ), indicating these populations are homogenous (Edwards, 1976). Therefore, the two variances were pooled to calculate broad-sense heritability (H) (Urrea et al., 2002). The estimates of H were quite high (0.62–0.81, Table 2). However, this result indicates that expression of resistance would be affected by environmental factors (Capettini et al., 2003) such as weather (Roger et al., 1999) and region (Faris-Mokaiesh et al., 1996).


Figure 1
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  		Figure 1. Distribution of disease reaction to mycosphaerella blight for four populations of F2:4 (2005) and F2:5 (2006) of Pisum sativum in field trials at Vegreville, AB, Canada (0 = no disease, 9 = severe blight).

 

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  		Table 2. Broad-sense heritability (H), realized heritability (h2), selection differential (S), standard phenotypic deviation ({sigma}P) and selection intensity (i), and response to selection (R) of resistance to Mycosphaerella pinodes detected from four crosses (F2:4 and F2:5 populations) of Pisum sativum at Vegreville, AB, Canada, in 2005 and 2006.

 
The distribution of mycosphaerella blight reaction of selected individuals and their developed families is shown in Fig. 2 . Estimates of narrow-sense heritability (h2) were moderate (0.43–0.57, Table 2), indicating that resistance to M. pinodes is a moderately heritable trait (Goodnight, 2000) and that additive genetic components contribute substantially to the genetic variance. We conclude that divergent individual selection in early generations would be an effective way to improve this trait.


Figure 2
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  		Figure 2. Distribution of disease reaction to mycosphaerella blight for selected individual plants in F2:4 (2005) and the developed family lines F4:5 (2006) in four crosses of Pisum sativum in field trials at Vegreville, AB, Canada (0 = no disease, 9 = severe blight).

 
Selection intensity (i), selection differential (S), and phenotypic deviation ({sigma}P) were also estimated (Table 2). Variation within these quantitative genetic parameters among the four populations is affected mainly by the frequency of alleles for resistance (Ågren and Schemske, 1992). Selection intensity and population size did not differ among the crosses, so the selection differential was influenced mainly by phenotypic deviation (de Souza et al., 2000; Hanrahan et al., 1973). The size of {sigma}P reflects the difference between the two parents that contributed resistance alleles (Mühlenbein and Schlierkamp-Voosen, 1995). For example, PI 203069 and PI 179449 have the greatest difference in reaction to mycosphaerella blight, and their offspring have the largest {sigma}P, S, and response to selection (R) of the four crosses (Table 2). Parental lines in a breeding program would likely have a smaller selection differential (more similar to CEB 1171/Radley), but we conclude that resistance to mycosphaerella blight can be improved by accumulating resistance alleles at a higher frequency in the offspring (Qian et al., 2000).

In contrast, the low selection differential in the cross Tara/JI 2480 was due to limited genetic differences for resistance in these highly susceptible parental lines (Table 2; Tar'an et al., 2003). This result indicates that development of field pea lines with improved resistance to M. pinodes will most likely result from crosses between the most resistant lines available.


   CONCLUSIONS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 CONCLUSIONS
REFERENCES
 
The disease reaction of progeny from crosses among lines of P. sativum that differ in resistance to M. pinodes ranged from highly susceptible to partially resistant. Significant additive genetic effects were detected, which indicates that genetic improvement based on progeny testing could be effective. Heritability analyses confirmed that resistance to M. pinodes is polygenic and moderately heritable. We conclude that resistance to M. pinodes can be improved by selection in early segregating generations from crosses among moderately susceptible parental lines of P. sativum.


   ACKNOWLEDGMENTS
 
We thank the Alberta Research Council for partial funding of the study, R. Gibson and P. Kharbanda for their advice, and G. Turnbull, J. Newman, and M. Mckenzie for excellent technical assistance.


   NOTES
TOP
 NOTES
ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 CONCLUSIONS
 REFERENCES
 
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Received for publication March 12, 2007.


   REFERENCES
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 CONCLUSIONS
 REFERENCES
 





This Article
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Right arrow Articles by Gossen, B. D.
Related Collections
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Right arrow Plant Disease

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