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ssss1 Breeding pyramid. A three‐tiered approach to breeding for yield in common bean.

Source: Kelly et al. (1998).

The choice of breeding systems is dictated by contrasting goals as well as the type of germplasm and the traits being improved. Having flexibility to change methods is critical due to the unpredictability of genetic recombination in certain crosses. Over the years, many breeders have identified specific genotypes/varieties not only as specific donor of economic traits but as good general combiners (i.e., they generally produce useful progeny). Other varieties that may be high yielding may prove to be poor general combiners, producing an array of mediocre progeny regardless of the other parents used in the cross. This information is only accumulated after years of experience of making crosses and from sharing similar information with breeder colleagues.

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.