Heritability of Resistance to White Mold in Snap Bean (Phaseolus vulgaris L.) Based on Field Evaluation, Oxalic Acid, and Straw Test Yong Suk Chung , Michell E. Sass, Scott C. Schaefer, James Nienhuis Department of Horticulture, University of Wisconsin – Madison Introduction Sclerotinia sclerotiorum (Lib.) de Bary (phylum Ascomycota) is a ubiquitous necrotrophic fungi that is a common pathogen in cool and wet environments worldwide (Purdy, 1979; Bolton et al., 2006). The disease has many common names depending upon host and symptoms, the most common include stem rot and white mold. White mold of dry bean (Phaseolus vulgaris L.) was first reported in 1944 in Colorado and Wyoming, but due to sporadic environmental conditions favorable to disease development and lack of inoculum, the disease was limited to localized outbreaks until early 1990’s (Dickson et al., 1982). Currently, white mold is an important production constraint to processing snap bean in the cool-wet northern states including Wisconsin. Objective The objective of this research is to estimate the heritability of white mold resistance based on both field and greenhouse evaluations in two snap bean populations derived using a common resistance parent. Materials and Methods The germplasm accession, ‘G122’, has over years and locations ranked among the most tolerant in the White Mold Cooperative nursery coordinated by Jim Steadman, University of Nebraska. G122 was used as the donor parent in the development of a recombinant inbred line population (Astrel x G122) in a cross to the small sieve snap bean cultivar ‘Astrel’. An independent inbred backcross population’TR781’ was developed by crossing and backcrossing to a large sieve snap bean, ‘PLS8088’. The two populations, A x G and TR781, represent theoretical contributions of 50 and 25 percent of the G122 genome, respectively. The two populations were evaluated over two years, 2004 and 2005, at the Arlington Agric. Res. Station, Arlington, WI, in a field inoculated with white mold sclerotia and mist irrigated. The populations were evaluated for disease incidence (percentage of plants in a row in which white mold symptoms were observed) and disease severity (the mean number or nodes affected in a sample of 10 plants). The populations were evaluated in the greenhouse for reaction to the oxalic acid toxin produced naturally by the white mold fungus. The populations were also evaluated using the straw test for the number of nodes that mycelial inoculum progressed over a three week period. Field Evaluation Greenhouse Evaluation Disease Incidence Disease Severity Oxalic Acid Test Straw Test Resistant and susceptible reactions to 20 mM oxalate solution (pH 4.0) Susceptible Resistant Scale 5: Stem/branch progression of fungus passed the first node Scale 7: Stem/branch progression of fungus to the second node Scale 9: Stem/branch progression to the third internode > 1 inch Modified scale of Petzoldt and Dickson (1996) for white mold rating in common bean Scale 3: Stem/branch infection of the first internode > 1 inch Results and Discussion All greenhouse and field evaluation methods distinguished among genotypes; however, the correlation among methods was low. Low correlation may be due to the fact that most greenhouse tests are based on the growth and development of mycelial infections, whereas the primary inoculum source in the field is ascospores (Kull et al., 2003) as well as due to avoidance mechanism. Marker assisted selection may be useful in selecting for architectural and physiological components of white mold resistance in snap bean. Figure 1. Distribution of two populations (Astrel x G122 and TR781) evaluated for white mold resistance using two greenhouse and two field based evaluation procedures. 1 0.00ns 67 0.27* 66 0.26* Straw Test 0.37** 60 0.10ns 0.06ns Oxalic Acid Test 0.31* 62 0.20ns 64 0.80*** Disease Severity 0.18ns 0.19ns 0.87*** Disease Incidence Table 2. Spearman correlation coefficients among two greenhouse tests, and two methods of field evaluation for resistance to white mold over years (A x G) is above diagonal, and TR781 is below diagonal). *, **, *** Significant at the 0.05, 0.01, and 0.001 probability level, respectively. ns = Nonsignificant at P < 0.05. References Bolton, M.D., B. Thomma, and B.D. Nelson. 2006. Sclerotinia sclerotiorum (Lib.) de Bary: biology and molecular traits of a cosmopolitan pathogen. Molecular Plant Pathology 7:1-16. Dickson, M.H., J.E. Hunter, M.A. Boettger, and J.A. Cigna. 1982. Selection for resistance in Phaseolus vulgaris L. to white mold disease caused by Sclerotinia sclerotiorum (Lib.) de Bary. J. Amer. Soc. Hort. Sci. 107:231-234. Kolkman J.M. and James D. Kelly. 2000. An indirect test using oxalate to determine physiological resistance to white mold in common bean. Crop Science 40:281-28520 Kull, L.S., T.D. Vuong, K.S. Powers, K.M. Eskridge, J.R. Steadman, and G.L. Hartman. 2003. Evaluation of resistance screening methods for Sclerotinia stem rot of soybean and dry bean. Plant Dis. 87:1471-1476. Petzoldt, R. and M.H. Dickson. 1996. Straw test for white mold disease in common beans. Annu. Rep. Bean Improv. Coop. 39:142-143 Purdy, L.H. 1979. Sclerotinia sclerotiorum: history, diseases and symptomatology, host range, geographic distribution, and impact. Phytopathology 69:875-880.