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Beans are attacked by a wide array of bacterial, fungal, and viral pathogens. Bean‐breeding programs that ignore disease resistance do so at their own peril, as many high‐yielding varieties are lost due to susceptibility to diseases. Most programs focus on the few major pathogens that are problematic in their local production areas, but some seed‐borne diseases such as Bean common mosaic virus (BCMV) are a universal problem, so all new varieties, regardless of production region, need to possess resistance. Rather than list all the pathogens that attack beans, and potential sources of resistance, the authors refer the reader to a few recent reviews on the subject (Miklas et al. 2006; Terán et al. 2009; Singh and Schwartz 2010). Two major types of disease resistance exist in beans and are broadly categorized into major single gene or qualitative resistance in contrast to partial resistance that is quantitatively inherited. Resistance to the highly specialized pathogens – such as bean anthracnose, bean rust, and BCMV – are controlled by major genes, whereas resistance to those pathogens such as Sclerotinia white mold that attack a broad array of crops is more complex. Breeders have identified many single‐resistance genes that control specific races (strains) of bean anthracnose (Kelly and Vallejo 2004), bean rust (Liebenberg and Pretorius 2010), and BCMV (Kelly et al. 2003). Molecular markers linked to these major genes have been developed that facilitate the pyramiding of multiple genes for resistance in single varieties as a way of increasing the durability (shelf life) of the resistance genes (Miklas et al. 2006; Kelly and Bornowski 2018). Recent progress has been made in identifying the actual proteins underpinning some of the resistance genes. For example, a truncated CRINKLY4 kinase conditions anthracnose resistance at the Co‐1 locus (Richard et al. 2021) and a mutated eIF4E translation initiation factor underlies the bc‐3 recessive gene for resistance to BCMV (Naderpour et al. 2010). These highly specialized pathogens have the ability to mutate and evolve new strains that overcome individual resistance genes, so breeders need to be vigilant for changes in pathogen virulence in order to deploy effective resistance genes in future varieties.

Resistance to those pathogens that cause root rots, white mold, and common bacterial blight (CBB) is only partial and is usually under large environmental effects. The partial resistance is quantitative in nature and QTL analysis is used to measure the size (effect) and chromosomal location of each locus that contributes to the overall resistance (Vasconcellos et al. 2017). Complete resistance is not possible to achieve, as many environmentally sensitive QTL contribute to resistance, and a large number of QTL need to be accumulated to provide effective resistance. Limited progress in breeding for resistance to these diseases has been reported, with the exception of CBB (Singh and Miklas 2015), where QTL with major effects have been identified (Viteri et al. 2014) and combined to achieve high levels of CBB resistance. The transfer of two major QTL from tepary to common bean is a major success story for interspecific hybridization using embryo rescue methods (Thomas and Waines 1984). The two major QTL exhibit recessive epistasis, and when combined confer a high level of resistance to CBB in common bean (Vandemark et al. 2008). A combination of single gene resistance to individual races (Miklas et al. 2014) with QTL conferring resistance to most races (Tock et al. 2017) has been used to breed for resistance to halo bacterial blight.