Three RFLP maps, as well as several RAPD maps have been developed in common bean (Phaseolus vulgaris L.). In order to align these maps, a core linkage map was established in the recombinant inbred population BAT93;Jalo EEP558 (BJ). This map has a total length of 1226 cM and comprises 563 markers, including some 120 RFLP and 430 RAPD markers, in addition to a few isozyme and phenotypic marker loci. Among the RFLPs mapped were markers from the University of California, Davis (established in the F of the BJ cross), University of Paris-Orsay, and University of Florida maps. These shared markers allowed us to Communicated by P. M. A. Tigerstedt

The product of the abrB gene of Bacillus subtilis is an ambiactive repressor and activator of the transcription of genes expressed during the transition state between vegetative growth and the onset of stationary phase and sporulation. Purified AbrB protein binds specifically in a highly co‐operative fashion to fragments of DNA containing the promoters it affects. DNase I footprints of the binding regions in these promoters revealed large protected areas of 50‐120 nucleotides or more depending on the promoter. Methylation protection experiments gave protected guanine residues on only one face of the DNA helix. A consensus sequence could be deduced around these guanine residues that was not found around non‐protected guanine residues in the footprint region. The results suggested that stationary phase functions and sporulation are repressed during active growth by AbrB and other transition state regulators by binding to the affected promoters in a concentration‐dependent manner.

Physiological resistance is an important component of integrated strategies used to control white mold [caused by Sclerotinia sclerotiorum (Lib.) de Bary], a major disease of common bean (Phaseolus vulgaris L.) in North America. Information pertaining to inheritance of physiological resistance, as detected by the greenhouse straw test, and its relationship with field resistance is lacking. The objectives of this study were to compare physiological resistance as detected by two separate straw tests with field resistance, evaluate heritability of physiological resistance, and to characterize the disease reaction of G 122 by quantitative trait locus (QTL) analysis. This was done in a recombinant inbred population (A 55/G 122) consisting of 67 F8‐derived lines. The greenhouse tests with five and six replications, respectively, and the field test with three replications were conducted in randomized complete block designs. Moderate heritability for disease reaction (scored from 1 = no symptoms to 9 = severe disease) was observed across the straw tests (0.65) and in the field (0.78). Inheritance of disease reaction was further investigated with a framework linkage map composed of 74 markers. Interval mapping detected a QTL on linkage group B7 near the phaseolin seed protein (Phs) locus that explained 38% of the phenotypic variation for disease score across the straw tests. 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, a measure of potential 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 to combat white mold disease.

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