White mold, caused by Sclerotinia sclerotiorum (Lib.) De Bary, is a serious yield reducing fungal pathogen of common bean (Phaseolus vulgaris L.). Our objective was to identify QTL for resistance to white mold from wild and landrace accessions of common bean using two inbred backcross line (IBL) populations derived from the recurrent black bean parent ÔTacanaÕ. Selective phenotyping failed to detect QTL for field disease resistance but other agronomic traits less sensitive to environmental conditions or population size were detected. Four novel QTLs for white mold resistance WM3.3 TW , WM7.5 TL , WM9.2 TW , and WM11.1 TL were identified in the greenhouse straw test on linkage groups B3, B7, B9, and B11, respectively, and two previously mapped QTL were also validated on B2 and B4. QTL, SY2.1 TL that accounted for 19-37% of the variation for yield under white mold pressure over 3 years, was detected on B2 in the TL population. Enhanced resistance to white mold in common bean could be achieved by combining different QTL associated with physiological resistance with yield under disease pressure.

Breeding for genetic resistance to white mold [Sclerotinia sclerotiorum (Lib.) de Bary] in dry bean (Phaseolus vulgaris L.) is difficult because of low heritability. To facilitate breeding, researchers have sought to identify QTL underpinning genetic resistance to white mold. We identified two QTL conditioning ICA Bunsi‐derived resistance to white mold in a pinto × navy bean (Aztec/ND88–106–04) recombinant inbred line (85 RILs) population. ND88–106–04 is a navy breeding line with resistance to white mold derived from ICA Bunsi navy. Aztec pinto is susceptible. The QTL were located to linkage groups B2 and B3 of the core map. The B2 QTL expressed in three of four field environments explaining 24.7, 9.0, and 8.7% of the phenotypic variation for disease severity score. The B3 QTL expressed in two of four environments, explaining 15.7 and 5.3% of the phenotypic variation. The B2 QTL was identified previously in ICA Bunsi × navy and ICA Bunsi × black bean RIL populations. The resistance conferred by the B2 QTL has a physiological basis due to association with stay green stem trait and lack of association with disease avoidance traits. The B3 QTL, undetected in previous studies, was associated with disease avoidance traits (canopy porosity, plant height), stay green stem trait, and maturity. The B2 QTL with stable expression in multiple environments and across genetic backgrounds will be most amenable to manipulation by breeders.

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Yield and quality losses due to disease are major factors limiting crop productivity; thus breeding for disease resistance is a primary goal for many plant breeding programmes. Unfortunately, specific sources of resistance are not always available. In cases where sources of genetic resistance are limited or non-existent, manipulating plant architecture to facilitate disease avoidance may be a valuable alternate approach to mitigate disease severity. Modifications of plant architecture can be used to reduce contact with the pathogen, create barriers to pathogen growth and development, or create an unfavourable microclimate for disease development. Architectural variants have long been observed by plant breeders and geneticists, and are frequently utilized to develop new plant types. Key variants that may facilitate disease control include altered plant height, determinacy, branching patterns, branch or leaf angle, flower position, organ coverage or shape, or root structure patterns. Implementing disease avoidance by an architectural approach requires an understanding of both the life cycle of the pathogen and the genetic basis for the desired morphological traits. This review examines examples where modified architecture can be employed to reduce disease. Among the better-documented cases are modified canopy structure to reduce white mould in dry bean and tightly closed ears to reduce Fusarium ear rot of maize. These examples demonstrate that breeding for modified plant architecture can be a valuable component of a broader disease control strategy that also includes genetic resistance and cultural and chemical controls.

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