|Johnson, William - CORNELL UNIV., NY|
|Gepts, Paul - UNIV. OF CA, DAVIS|
Submitted to: Crop Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 1, 2000
Publication Date: January 1, 2001
Citation: MIKLAS, P.N., JOHNSON, W.C., DELORME, R.M., GEPTS, P. IDENTIFICATION OF QTL CONDITIONING PHYSIOLOGICAL RESISTANCE AND AVOIDANCE TO WHITE MOLD IN DRY BEAN G 122 (PI 163120). CROP SCIENCE, 41:309-315. 2001. Interpretive Summary: Sclerotinia white mold is the most important disease of common bean in the U.S. Yield and quality losses combined with chemical fungicides used to control the disease cost growers up to $30 M annually in lost income. The use of plant breeding to improve genetic resistance to control this disease has just begun in most bean programs across the U.S. This report is the first to describe inheritance and genomic locations of genes conditioning physiological resistance and avoidance to white mold derived from the Plant Introduction 163120. The information generated will assist breeders in the development of white mold resistant cultivars. Eventual release of cultivars with improved resistance to white mold will significantly reduce the amount of lost grower income resulting from this disease, and reduce environmental impact of the disease due to reduced pesticide use.
Technical Abstract: Physiological resistance is an important component of integrated strategies used to control Sclerotinia white mold disease of common bean in North America. Information pertaining to the mode of inheritance of physiological resistance, as detected by the greenhouse straw test, and its relationship with field resistance is lacking. We compared physiological resistance as detected by two separate straw tests with field resistance in a recombinant inbred population (A 55/G 122) consisting of 67 F8-derived lines. Moderate heritability for disease reaction (scored from 1 to 9) was observed in the straw tests (0.60 and 0.61) and field (0.64). Inheritance of disease reaction was further investigated with a framework linkage map composed of 74 markers. Interval mapping detected a quantitative trait locus (QTL) on linkage group B7 near the phaseolin seed protein (Phs) locus that explained 36 and 35% of the phenotypic variation for disease score across each straw test. The same B7 QTL (26%), and an additional QTL (18%) on B1 near the fin gene for determinate growth habit, conditioned field resistance. A QTL (34%) for canopy porosity, used to measure potential for disease avoidance, also mapped to the fin locus. Results confirmed that physiological resistance as detected by the straw test was an integral component of field resistance, and that both physiological and avoidance mechanisms contributed to field resistance in the A 55/G 122 population. The landrace G 122 clearly provides breeders with a heritable source of physiological resistance and avoidance to combat white mold disease.