HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Free Alert me when this article is cited Alert me if a correction is posted Services Related articles in Crop Science Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Van Becelaere, G. Articles by Miller, J. F. Search for Related Content PubMed Articles by Van Becelaere, G. Articles by Miller, J. F. Agricola Articles by Van Becelaere, G. Articles by Miller, J. F. Related Collections Sunflower Plant Disease Crop Genetics

CROP BREEDING, GENETICS & CYTOLOGY

Combining Ability for Resistance to Sclerotinia Head Rot in Sunflower

^a Dep. of Plant Sciences, North Dakota State Univ., P.O. Box 5051
^b USDA-ARS, Northern Crop Science Lab., P.O. Box 5677, Fargo, ND 58105

^* Corresponding author (millerjf{at}fargo.ars.usda.gov).

	ABSTRACT

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
Sclerotinia head rot, caused by Sclerotinia sclerotiorum (Lib.) de Bary, is a major disease in sunflower (Helianthus annuus L.). The development of hybrids with adequate genetic resistance is necessary to reduce yield losses caused by this disease. The objective of this study was to estimate the general (GCA) and specific (SCA) combining ability of a set of female and male oilseed sunflower inbred lines in hybrid combinations for resistance to Sclerotinia head rot. Six female and six male lines were crossed in a factorial mating design. The hybrids were planted in three U.S. environments and in Argentina. Plants were inoculated with a suspension containing 5000 ascospores per milliliter. Sclerotinia head rot disease incidence was measured as percentage of plants attacked on a plot basis. The GCA effects accounted for a greater proportion of the treatment sum of squares than the SCA effects, suggesting that additive gene effects were relatively more important than nonadditive gene effects in the phenotypic expression of resistance to Sclerotinia head rot. The importance of additive gene effects suggests that selection could start at the inbred line development stage. However, hybrids should also be tested since nonadditive gene effects were significant in the individual environments and certain hybrid combinations showed higher or lower disease incidence than would be expected based on the average performance of their parents.

Abbreviations: GCA, general combining ability • SCA, specific combining ability

	INTRODUCTION

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
SCLEROTINIA SCLEROTIORUM is one of the most important pathogens of sunflower and is encountered in all sunflower-growing regions of the world (Gulya et al., 1997). It is a facultative parasite and has a vast host range, including more than 400 species. The fungus can attack several plant parts and causes two major diseases, stalk rot or wilt and head rot. Sclerotinia head rot is considered a major disease in Europe, Argentina, and the USA.

The initial symptom of Sclerotinia head rot is the appearance of white mycelia covering the developing seed. Under favorable conditions, the mycelia extend to the dorsal surface of the head and tan water-soaked lesions appear. The fungus rots the interior of the capitulum, leaving only the vascular elements after a severe attack. Severe attacks can cause losses up to 100% (Sackston, 1992).

There are no effective chemical controls available to apply on a large scale (Péres and Regnault, 1985). Thus, the development of hybrids with adequate genetic resistance is necessary. Although complete resistance in cultivated sunflower has not been reported, significant differences in the level of susceptibility have been identified in diverse germplasm (Leclerq, 1973). The degree of infection is affected by the presence of sclerotia in the soil and weather conditions; for that reason, field testing under natural infection generally shows variable results. Breeders cannot rely only on observations under natural attack for selection of resistant plants across generations. Inoculation techniques that simulate the conditions of natural infection are needed to screen for resistance. Ascospore and mycelium tests have been demonstrated to be useful for detecting differences among sunflower genotypes for resistance to Sclerotinia sclerotiorum attacks on the head (Tourvieille and Vear, 1984; Vear and Guillaumin, 1977).

Genotypes differed in their behavior during each phase of the infection process and had independent reactions according to the plant part attacked (Thuault and Tourvieille, 1988). Resistance to stem wilt was not necessarily correlated with resistance to head rot, suggesting that different genetic factors were involved (Gulya et al., 1997). According to Mestries et al. (1996), each form of attack should be considered a different disease and breeding should be simultaneous to obtain cultivars or hybrids with a good level of overall resistance.

There are two types of resistance to Sclerotinia head rot in sunflower (Castaño et al., 1993) which correspond to the two phases of infection: resistance to penetration of the fungus into the plant and resistance to extension of the mycelia in the parenchymal tissue. Resistance to Sclerotinia sclerotiorum attacks in the head was polygenic, with additive effects being relatively more important than dominant effects (Godoy et al., 2000; Robert et al., 1987; Vear and Guillaumin, 1977; Vear and Tourvieille, 1988). The resistance of the inbred lines per se measured by artificial infections usually provided a good estimation of the resistance shown by their hybrids (Robert et al., 1987; Vear and Tourvieille, 1988).

The amount of variation in the germplasm due to genetic differences and the importance of each type of gene action involved in the expression of the resistance are of special interest for the breeder to select the best strategy for developing resistant cultivars or hybrids. The objective of this study was to estimate the GCA and SCA of a set of female and male oilseed sunflower inbred lines in hybrid combinations for resistance to Sclerotinia head rot.

	MATERIALS AND METHODS

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
Six sunflower male sterile lines were used as female parents and crossed to six restorer lines used as male parents in a factorial mating design. The female parents were HA 89 (PI 599773), HA 372 (PI 534658), HA 410 (PI 603991), HA 412 (PI 603993), HA 821 (PI 599984), and HA 441 (released by USDA-ARS, 4 April 2003, registration pending); the male parents were RHA 274 (PI 599759), RHA 373 (PI 560141), RHA 377 (PI 560145), RHA 409 (PI 603990), RHA 801 (PI 599768), and PSC8. All lines were USDA-ARS germplasm releases except PSC8, which was obtained from the Station d'Amelioration des Plantes, INRA, Clermont-Ferrand, France. These genotypes were selected based on their variability in reaction to natural infection of Sclerotinia head rot in previous breeding nurseries in North Dakota. The hybrid HA 89 x RHA 274 is known as ‘894’ and served as a long-term check.

The experimental design was a randomized complete block design with three replications. Each plot consisted of a single 6-m row with a spacing of 75 cm between rows. Plants were thinned by hand to a spacing of approximately 30 cm between plants. The experiments were planted at Fargo and Carrington, ND, in 2001 and 2002. The planting date at Fargo was 24 May in both years while at Carrington, in 2001, the planting date was 29 May. The experiment at Carrington in 2002 was lost because of a severe storm; for that reason, an additional experiment was planted at Junín, Argentina, on 9 Dec. 2002.

Ten heads per plot were inoculated with a suspension containing 5000 ascospores per milliliter of distilled water. The concentration of ascospores was measured with a hemocytometer. A total of 5 mL was applied to each head. The heads were sprayed at the beginning of flowering, stage R5.1 (Schneiter and Miller, 1981); and all heads within each plot were inoculated on the same day. In Fargo, inoculated heads were covered with brown paper bags immediately after being sprayed. In Carrington and Argentina, mist irrigation commenced after inoculation. Infection was measured on inoculated heads 35 d after inoculation. The variable analyzed was disease incidence, measured as percentage of plants attacked on a plot basis.

The treatment sum of squares was partitioned into the variation due to females (i), males (j), and the female x male interaction. The main effects of the female and male lines are equivalent to the GCA effects, and the female x male interaction is equivalent to the SCA effects (Hallauer and Miranda, 1981). Analyses of variance were performed using PROC GLM (SAS Institute, 1990). The homogeneity of error variances of individual environments was tested by Bartlett's chi-square test (Steel et al., 1997). The female and male lines were considered fixed effects whereas environment was considered a random effect. Missing plots were estimated by using the method proposed by Yates (Cochran and Cox, 1957). Kendall's coefficient of concordance (Daniel, 1990) was calculated to determine if the treatment x environment interaction was mainly due to changes in magnitude or to rank order changes.

The GCA effect for each female and male line and the SCA effect for each cross were calculated as follows:

where _i. is the mean of hybrids with the ith female line averaged across males, replicates, and environments; _.j is the mean of hybrids with the jth male line averaged across females, replicates, and environments; _ij is the mean of the hybrid with the ith female line and the jth male line, averaged across replicates and environments; and _.. is the overall mean.

Standard errors for the GCA effects of female and male lines and standard errors for the SCA effects of the crosses were calculated by the method described by Cox and Frey (1984). Two-tailed t tests were performed to test the significance of GCA and SCA effects, where t = GCA/SE_GCA or SCA/SE_SCA, respectively.

	RESULTS AND DISCUSSION

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
The error variances of the four environments for Sclerotinia head rot disease incidence were not homogeneous. However, the error variances of the three U.S. environments were homogeneous; thus, the U.S. environments were combined and the experiment in Argentina was analyzed separately.

U.S. Environments
The disease incidence grand mean of plants infected with Sclerotinia sclerotiorum after inoculation was 28%, and the coefficient of determination was 0.79. The treatment x environment interaction was significant (Table 1). However, Kendall's coefficient of concordance was 0.65 and the ² approximation was 67.83, indicating that the treatment x environment interaction was due mainly to changes in magnitude and not to rank order changes. Therefore, the combined analysis will be discussed.

The GCA effects of the female lines were nominally greater than the GCA effects of the male lines (Table 1), but it is difficult to determine to what extent this difference was genetically meaningful. The female line HA 441 and the male line PSC8 had significant, negative GCA effects (Table 2). The male line RHA 409 had a significant, positive GCA effect. Large negative GCA values indicated greater resistance, and large positive GCA values indicated greater susceptibility.

Argentina, 2002–2003
The disease incidence experimental mean of plants infected with Sclerotinia sclerotiorum after inoculation was 82%, and the coefficient of determination was 0.67. The disease incidence was considerably higher than in the U.S. environments because of more humid conditions during and after flowering.

The GCA effects of both female and male lines, as well as the SCA effects, were significant (Table 3). The GCA effects of the female and male lines accounted for 67% of the treatment sum of squares, suggesting that additive gene effects were relatively more important than nonadditive gene effects in the phenotypic expression of disease incidence.

Conclusions
The GCA effects accounted for a greater proportion of the treatment sum of squares for disease incidence than the SCA effects, suggesting that additive gene effects were relatively more important than nonadditive gene effects in the phenotypic expression of resistance to Sclerotinia head rot. These results agreed with those obtained by Robert et al. (1987) and Vear and Guillaumin (1977) with the mycelium test, and with those obtained by Godoy et al. (2000) and Vear and Tourvieille (1988) with the ascospore test. Nevertheless, since the genotypes were considered fixed effects, the conclusions of this study cannot be extrapolated to other sets of lines or hybrids. The importance of the GCA effects suggests that selection could start at the inbred line development stage. However, hybrids should also be tested since the SCA effects were significant in the individual environments and certain hybrid combinations showed higher or lower disease incidence than would be expected based on the average performance of their parents. Selection should be done based on families rather than on single plants and especially by discarding those families with the worst performance.

This study identified female and male oilseed sunflower inbred lines that could be used in a breeding program to develop hybrids with reasonably high levels of resistance that could provide protection from Sclerotinia head rot in producer fields. The female line HA 441 and the male line PSC8 had significant, negative GCA effects in all environments; therefore, their use as sources of resistance to Sclerotinia head rot in a breeding program is recommended. The hybrid HA 441 x PSC8 had the lowest disease incidence in all environments and a significant, negative SCA effect in Argentina; however, it did not have a significant SCA effect in the U.S. environments. The SCA effects of crosses between lines with high levels of resistance were probably underestimated in environments with low levels of infection.

	ACKNOWLEDGMENTS

 
This study would not have been possible without the Gerhardt Fick Foundation Charitable Gift Fund. The authors thank Dr. James J. Hammond, Plant Science Department, North Dakota State University, for his consultation regarding the statistical analysis. The authors also thank Dale Rehder, Dr. Tom Gulya, Scott Radi, Robert MacArthur, and Robert Henson for their assistance in this study.

	NOTES

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 
Part of a dissertation submitted by G. Van Becelaere in partial fulfillment of the requirements for a Ph.D. degree. Financial support was provided by the Gerhardt Fick Foundation Charitable Gift Fund.

Received for publication October 7, 2003.

	REFERENCES

TOP NOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS AND DISCUSSION REFERENCES

 

• Castaño, R.F., F. Vear, and D. Tourvieille. 1993. Resistance of sunflower inbred lines to various forms of attack by Sclerotinia sclerotiorum and relations with some morphological characters. Euphytica 68:85–98.
• Cochran, W.G., and G.M. Cox. 1957. Experimental designs. 2nd ed. John Wiley & Sons, New York.
• Cox, D.J., and K.J. Frey. 1984. Combining ability and the selection of parents for interspecific oat matings. Crop Sci. 24:963–967.[Abstract/Free Full Text]
• Daniel, W.W. 1990. Applied nonparametric statistics. 2nd ed. Wadsworth, Boston.
• Godoy, M., F. Castaño, J. Ré, R. Rodríguez, and A. Escande. 2000. Sunflower white rot incidence: Combining ability of inbred lines and relative performance of hybrids in two environments. p. 42–47. In Proc. 15th Int. Sunflower Conf., Toulouse, France. 12–15 June 2000. Int. Sunflower Assoc., Paris.
• Gulya, T., K.Y. Rashid, and S.M. Marisevic. 1997. Sunflower diseases. p. 263–379. In A.A. Schneiter (ed.) Sunflower technology and production. Agron. Monogr. 35. ASA, CSSA, and SSSA, Madison, WI.
• Hallauer, A.R., and J.B. Miranda. 1981. Quantitative genetics in maize breeding. Iowa State Univ. Press, Ames.
• Leclerq, P. 1973. Influence de facteurs héréditaires sur la résistance apparente du tournesol à Sclerotinia sclerotiorum. Ann. Amélior. Plantes 23:279–286.
• Mestries, E., F. Vear, and D. Tourvieille. 1996. Resistance of sunflowers to extension of Sclerotinia sclerotiorum mycelium on leaves and capitula. p. 50–55. In Proc. 14th Int. Sunflower Conf., Symposium I, Beijing, China. 12–20 June 1996. Int. Sunflower Assoc., Paris.
• Péres, J., and Y. Regnault. 1985. Sclerotinia sclerotiorum (Lib.) de Bary: Recherche de moyens chimiques permettant de limiter la production d'inoculum par traitement du sol. p. 363–368. In Proc. 11th Int. Sunfl. Conf., Mar del Plata, Argentina. 10–13 March 1985. Int. Sunflower Assoc., Paris.
• Robert, N., F. Vear, and D. Tourvieille. 1987. L'hérédité de la résistance à Sclerotinia sclerotiorum (Lib.) de Bary chez le tournesol. I. Etude des réactions à deux tests mycéliens. Agronomie 7:423–429.
• Sackston, W.E. 1992. On a treadmill: Breeding sunflowers for resistance to disease. Annu. Rev. Phytopathol. 30:529–551.[Web of Science]
• SAS Institute. 1990. SAS user's guide: Statistics. 4th ed. SAS Inst., Cary, NC.
• Schneiter, A.A., and J.F. Miller. 1981. Description of sunflower growth stages. Crop Sci. 21:901–903.[Abstract/Free Full Text]
• Steel, R.G.D., J.H. Torrie, and D.A. Dickey. 1997. Principles and procedures of statistics: A biometrical approach. 3rd ed. McGraw-Hill, New York.
• Thuault, M.C., and D. Tourvieille. 1988. Etudes du pouvoir pathogène de huit isolats de Sclerotinia appartenant aux espèces S. sclerotiorum, S. minor et S. trifoliorum sur le tournesol. Int. Tech. CETIOM 103:21–27.
• Tourvieille, D., and F. Vear. 1984. Comparaison de méthodes d'estimation de la résistance du tournesol à Sclerotinia sclerotiorum (Lib.) de Bary. Agronomie 4:517–525.
• Vear, F., and J.J. Guillaumin. 1977. Etude de méthodes d'inoculation du tournesol par Sclerotinia sclerotiorum et application à la sélection. Ann. Amélior. Plantes 27:523–537.
• Vear, F., and D. Tourvieille. 1988. Heredity of resistance to Sclerotinia sclerotiorum in sunflowers. II. Study of capitulum resistance to natural and artificial ascospore infections. Agronomie 8:503–508.

Related articles in Crop Science:

THIS ISSUE IN CROP SCIENCE

Crop Science 2004 44: 1507-1510. [Full Text]  

This article has been cited by other articles:

				J. M. Bokmeyer, S. A. Bonos, and W. A. Meyer Inheritance Characteristics of Brown Patch Resistance in Tall Fescue Crop Sci., October 22, 2009; 49(6): 2302 - 2308. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Free Alert me when this article is cited Alert me if a correction is posted Services Related articles in Crop Science Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Van Becelaere, G. Articles by Miller, J. F. Search for Related Content PubMed Articles by Van Becelaere, G. Articles by Miller, J. F. Agricola Articles by Van Becelaere, G. Articles by Miller, J. F. Related Collections Sunflower Plant Disease Crop Genetics