Tan spot is an economically important fungal disease of wheat that occurs globally. In this necrotrophic pathosystem, pathogen effectors are recognized by wheat genes in an inverse gene-for-gene manner, leading to the hijacking of host defense mechanisms and ultimately disease susceptibility. Here, we identified the tan spot susceptibility gene Tsc2 through positional cloning, mutagenesis, and transgenic complementation. Tsc2 encodes a diverged form of the exocyst subunit Exo70FX15 that localizes to the nucleus and cytoplasm and does not interact directly with the fungal effector. A 21‑nucleotide deletion in Tsc2 occurred in durum wheat more than a century ago and subsequently spread to common wheat through breeding practices, which allowed recognition of the pathogen effector and subsequent hijacking of the host immune system. We demonstrate that elimination of Tsc2 through conventional breeding using a diagnostic marker or disruption of Tsc2 by gene editing can be used to improve tan spot resistance in wheat. Tan spot is an economically important disease of wheat. Here the authors show that a deletion in the wheat gene Tsc2, which encodes an Exo70-like protein, enables a fungal effector to hijack host immunity causing cell death and demonstrate practical routes to tan spot resistance.

Identification of Rk candidate gene and diagnostic markers enabled precise introduction of the slow‑darkening (SD) allele into pink beans, producing stable SD phenotypes and expanding breeding utility across market classes. Common bean (Phaseolus vulgaris L.) is a globally important and nutritious crop with diverse market classes. Multiple genes control the seed coat color and patterns that characterize these market classes. Therefore, understanding the genetic control of seed coat color is critical for breeding purposes, especially when making crosses among different market classes. One such gene is Rk, the “red kidney” color gene. The recessive rkp allele controls the characteristic color expression of the pink market class. Through GWAS analysis, sequencing candidate genes across multiple market classes, genetic mapping, and phylogenetic analysis, we determined the gene model PvUI111.02G213800, which encodes anthocyanidin reductase, is the most likely candidate for the Rk gene. Pink beans, along with several other market classes, suffer from postharvest seed coat darkening, a quality issue that causes significant economic losses and reduces consumer appeal and nutritional value. The recessive Psd allele present in some pinto genotypes imparts a “slow-darkening” (SD) phenotype. To introduce the Psd allele into the pink market class, crosses were made between three pink beans and the SD pinto cultivar ND Palomino. Among 2240 F2 plants screened using PACE markers targeting multiple genes (Psd, rkp, and pi) controlling pink color and slow-darkening, 32 individuals exhibited the desired alleles and SD pink genotype. The SD phenotype was verified via ultra-violet (UV) testing (λ = 254 nm), and field trials of F5 generation lines demonstrated their phenotypic stability. Parallel efforts are underway to incorporate the SD trait into light red kidney and cranberry beans, broadening its utility across market classes.

Seed coat color and patterning are key quality traits in common bean (Phaseolus vulgaris L.) that define market classes and strongly influence consumer preference and market value. These traits are controlled by a complex network of major genes (sometimes with epistatic interactions), which complicates the recovery of desired market class phenotypes following inter-market class hybridization. Although many of the underlying loci have been genetically mapped, diagnostic, high-throughput molecular markers for efficient allele tracking across the Middle American and Andean gene pools remain limited. In this study, we developed and validated 24 gene-specific PCR Allele Competitive Extension (PACE) markers targeting seven major seed coat color genes (G, B, V, J, Rk, T, and Z) and two patterning genes (CPi and CSt), together with a previously reported marker associated with the postharvest seed coat darkening locus (Psd). An additional PACE marker targeting the Phaseolin (Phs) locus was developed to distinguish Middle American (S-type) and Andean (T-type) gene pools, providing a complementary tool for assessing genetic background alongside seed coat-specific loci. Marker performance was evaluated across three diverse panels, revealing high diagnostic accuracy for most loci (90%-100%). However, for loci such as J, V, Rk, T, and Z, allele-specific markers or marker combinations were required to capture full allelic diversity. Haplotype analysis further revealed substantial allelic diversity across market classes and identified background-specific interactions. Collectively, these results provide a comprehensive set of high-resolution, gene-anchored PACE markers for seed coat color, patterning, and gene pool classification in common bean. These markers enable rapid and precise allele tracking in breeding populations and germplasm collections, facilitating marker-assisted selection for market class-specific seed coat traits and accelerating genetic improvement.

Domestication imposed radically different selection pressures on plants, eventually transforming them into the cultivated forms that support global populations today. Here, we investigate the loss of seed dispersal via pod shattering during common bean ( Phaseolus vulgaris L.) domestication. We identified an eight-kb deletion eliminating the transcription start site and promoter of the candidate gene PvMYB26 . Mutants express PvMYB26 at < 1% of the level of wild types and produce 44% less pod lignin. Whole-genome sequencing revealed that the mutation is nearly diagnostic for domestication status among Middle American common bean, indicating its importance in domestication. We also identified a high-frequency PvMYB26 frameshift/premature stop mutation unique to Andean domesticates. Wild haplotypes most like Middle American domesticates are found in eastern Jalisco, Mexico. Our results suggest that West-Central Mexico was the site of common bean domestication and suggest that this region may have been important in the rise of Middle American agriculture. ### Competing Interest Statement The authors have declared no competing interest. Kirkhouse Trust, https://ror.org/00986jy03, A23-1518-001 USDA-NIFA-AFRI, 2023-67013-40001 California Agricultural Experiment Station, Davis, CA, USA, CA-D-PLB-2850-H California Agricultural Experiment Station, Davis, CA, USA, CA-D-PLS-2851-CG

Common bean (Phaseolus vulgaris L.) market classes have distinct seed coat colors, which are directly related to the diverse flavonoids found in the mature seed coat. To understand and elucidate the molecular mechanisms underlying the regulation of seed coat color, RNA-Seq data was collected from the black bean 5-593 and used for a differential gene expression and enrichment analysis from four different seed coat color development stages. 5-593 carries dominant alleles for 10 of the 11 major genes that control seed coat color and expression and has historically been used to develop introgression lines used for seed coat genetic analysis. Pairwise comparison among the four stages identified 6,294 differentially expressed genes (DEGs) varying from 508 to 5,780 DEGs depending on the compared stages. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that phenylpropanoid biosynthesis, flavonoid biosynthesis, and plant hormone signal transduction comprised the principal pathways expressed during bean seed coat pigment development. Transcriptome analysis suggested that most structural genes for flavonoid biosynthesis and some potential regulatory genes were significantly differentially expressed. Further studies detected 29 DEGs as important candidate genes governing the key enzymatic flavonoid biosynthetic pathways for common bean seed coat color development. Additionally, four gene models, Pv5-593.02G016100, 593.02G078700, Pv5-593.02G090900, and Pv5-593.06G121300, encode MYB-like transcription factor family protein were identified as strong candidate regulatory genes in anthocyanin biosynthesis which could regulate the expression levels of some important structural genes in flavonoid biosynthesis pathway. These findings provide a framework to draw new insights into the molecular networks underlying common bean seed coat pigment development.

The common bean weevil [Acanthoscelides obtectus (Say)] (AO) is the most important post-harvest pest of common bean (Phaseolus vulgaris L.) worldwide. Identifying sources of AO resistance and resistance loci is critical to developing resistant varieties. The Andean Diversity Panel (ADP) comprised of landraces, breeding lines and varieties from various countries and breeding programs is a major genetic and breeding resource of common bean. There are no previous efforts to understand the extent of genetic variability in the ADP for AO resistance and genetic basis of that possible resistance. The objectives of this study were to: (i) identify Andean genotypes resistant to AO, and (ii) identify genomic regions associated with AO resistance. The ADP (n = 476) was evaluated for resistance to AO. Number of perforations on the seed and percentage of damaged seed were recorded and used as metrics for AO resistance. The ADP was genotyped with 24,772 SNPs and genome-wide association analysis was conducted. Significant variability for AO resistance was observed in the ADP. A total of 15 accessions in variable market classes showed AO resistance. These 15 accessions can be used as sources of resistance to enhance AO resistance in specific market classes of common bean. Genomic regions on Pv03 and Pv07 with coefficient of determination (R2) of 14.2

Domestication imposed radical selection pressures on plants, transforming them into crops that support global populations today. In this study, we investigate the loss of seed dispersal via pod shattering during common bean (Phaseolus vulgaris L.) domestication. We identified PvMYB26 mutations in all three main gene pools of common bean, including an 8 kb deletion in Middle American lines eliminating the gene's transcription start site and promoter, a frameshift/truncation deletion in the independently domesticated Andean population, and another frameshift/truncation insertion in the genetic background of the "undomesticated" debouckii population. Mutants with the 8 kb deletion express PvMYB26 at <1% of the level of wild types and produce 44% less pod lignin. RNA in situ hybridization and fluorescence microscopy showed that PvMYB26 is expressed in the lignified fiber layer of pods, while mutants showed no visible expression and a greatly reduced fiber layer. Sequencing of 327 accessions revealed that the mutation is nearly diagnostic for domestication status among Middle American common bean and identified a 125 kb hard selective sweep, indicating the gene's importance in domestication. The main Andean frameshift mutation was found in 84.5% of Andean domesticates but 0% of wild lines, while the debouckii truncation was identified in six domesticated lines of race Peru, suggesting that a third proto-domestication of common bean may have occurred in Ecuador and/or northern Peru. Wild haplotypes most like Middle American domesticates were found in eastern Jalisco, Mexico, strongly suggesting west-central Mexico as the site of common bean domestication and the rise of agriculture in Middle America.

White mold, caused by the fungus Sclerotinia sclerotiorum (Lib.) de Bary, is a devastating disease affecting common bean (Phaseolus vulgaris L.) production worldwide. Breeding for resistance to white mold is challenging due to its quantitative inheritance and intricate genetic mechanisms. This research aimed to validate and characterize physiological resistance in the pinto dry bean market class through greenhouse straw tests under controlled conditions and field assessments under natural environments. Classical quantitative trait locus (QTL) mapping and Khufu de novo QTL-seq were employed to detect and narrow QTL intervals and identify candidate genes associated with white mold resistance in two pinto bean recombinant inbred line populations, PT9-5-6/USPT-WM-12 (P2) and PT12-37/VCP-13 (P3). Eleven QTL, five in P2 and six in P3, conditioning white mold resistance were identified. New QTL were discovered including WM1.4 and WM11.5 in P2, and WM1.5 and WM7.7 in P3. Existing major-effect QTL were validated: WM5.4 (34%-phenotypic variation explained) and WM7.4 (20%) in straw tests, and WM2.2 (15%) and WM3.1 (27%) under field conditions. QTL for avoidance traits such as resistance to lodging and late maturity overlapped WM2.2 in P2 and WM1.5, WM3.1, WM5.4, and WM7.7 in P3. WM5.4 (Pv05: 7.0-38.7 Mb) was associated with a large Phaseolus coccineus L. genome introgression in the resistant parent VCP-13. These findings offer narrowed genomic intervals and putative candidate genes for marker-assisted selection targeting white mold resistance improvement in pinto beans.

The Middle American rust resistance gene Ur-11 present in common bean (Phaseolus vulgaris L.) confers resistance to all but one known race of the pathogen Uromyces appendiculatus (Pers.) Unger. Even though progress has been made in understanding the host–pathogen interactions between common bean and U. appendiculatus, the causal alleles of the majority of rust resistance loci, including Ur-11, remain unknown. A genome-wide association study (GWAS) was conducted to identify genomic regions associated with resistance to the U. appendiculatus race 31–22, which is avirulent to Ur-11 but virulent to other Middle American rust resistance genes. GWAS using genotypic data consisting of approximately 70,959 SNP markers and phenotypic data based on the median reaction type (1–9 scale) of a panel of 357 Middle American breeding lines and cultivars, plus 5 germplasm lines with the Ur-11 locus derived from PI 181996, located Ur-11 on chromosome Pv11. Twenty-seven SNP markers clustered in the 55.16–55.56 Mb region of the P. vulgaris UI111 reference. Multiple DNA sequence alignments detected a missense mutation [c.1,328A > G] in the PvUI111.11G202400 gene model that encodes a leucine-rich repeat-containing protein in response to race 31–22. A PCR allele competitive extension marker (PACE) was developed and tested across a panel of 700 Middle American dry bean genotypes. No recombination event was observed for the PACE marker among the tested genotypes; suggesting that the polymorphism on which it is based is very close to or in the Ur-11 gene. This PACE marker will be a useful and reliable marker for marker-assisted selection of Ur-11-based resistance to bean rust.

ABSTRACTThe common bean weevil (Acanthoscellides obtectus [Say]) is a major post‐harvest pest of common bean (Phaseolus vulgaris L.) in tropical regions. Developing and using weevil‐resistant varieties is the most environmentally and cost‐effective means of mitigating the losses caused by the common bean weevil. The arcelin–phytohemagglutinin–alpha‐amylase (APA) locus, originally from tepary bean (Phaseolus acutifolius A. Gray), provides effective resistance against the common bean weevil. The APA locus is currently deployed in very limited market classes, and knowledge of the stability of its resistance across different market classes of common bean is limited. The objectives of this study were to (i) introgress the APA locus into selected market classes of Andean gene pool of common bean and (ii) determine the stability of APA‐based resistance to A. obtectus (AO) in multiple market classes of common bean. A total of 571 F5:7 breeding lines derived from crossing the weevil‐resistant breeding line AO‐1012‐29‐3‐3A (AO‐3A) possessing the APA locus with seven Andean genotypes belonging to five market classes were evaluated for resistance to AO. Of the 571 breeding lines screened, 16 were resistant, representing a low weevil resistance recovery rate of 2.8%. These lines are across diverse market classes, including those preferred in African countries. Of the 16 newly developed resistant breeding lines, six were more resistant to AO (scores ranging from 1–1.3) than AO‐3A (score of 2), and these can be used for further genetic enhancement of common bean resistance to AO.

Septoria nodorum blotch (SNB), caused by Parastagonospora nodorum, is a disease of durum and common wheat initiated by the recognition of pathogen-produced necrotrophic effectors (NEs) by specific wheat genes. The wheat gene Snn1 was previously cloned, and it encodes a wall-associated kinase that directly interacts with the NE SnTox1 leading to programmed cell death and ultimately the development of SNB. Here, sequence analysis of Snn1 from 114 accessions including diploid, tetraploid, and hexaploid wheat species revealed that some wheat lines possess two copies of Snn1 (designated Snn1-B1 and Snn1-B2) approximately 120 kb apart. Snn1-B2 evolved relatively recently as a paralog of Snn1-B1, and both genes have undergone diversifying selection. Three point mutations associated with the formation of the first SnTox1-sensitive Snn1-B1 allele from a primitive wild wheat were identified. Four subsequent and independent SNPs, three in Snn1-B1 and one in Snn1-B2, converted the sensitive alleles to insensitive forms. Protein modeling indicated these four mutations could abolish Snn1-SnTox1 compatibility either through destabilization of the Snn1 protein or direct disruption of the protein-protein interaction. A high-throughput marker was developed for the absent allele of Snn1, and it was 100% accurate at predicting SnTox1-insensitive lines in both durum and spring wheat. Results of this study increase our understanding of the evolution, diversity, and function of Snn1-B1 and Snn1-B2 genes and will be useful for marker-assisted elimination of these genes for better host resistance.

The aim of this study was to evaluate the accuracy of the ridge regression best linear unbiased prediction model across different traits, parent population sizes, and breeding strategies when estimating breeding values in common bean (Phaseolus vulgaris). Genomic selection was implemented to make selections within a breeding cycle and compared across five different breeding strategies (single seed descent, mass selection, pedigree method, modified pedigree method, and bulk breeding) following 10 breeding cycles. The model was trained on a simulated population of recombinant inbreds genotyped for 1010 single nucleotide polymorphism markers including 38 known quantitative trait loci identified in the literature. These QTL included 11 for seed yield, eight for white mold disease incidence, and 19 for days to flowering. Simulation results revealed that realized accuracies fluctuate depending on the factors investigated: trait genetic architecture, breeding strategy, and the number of initial parents used to begin the first breeding cycle. Trait architecture and breeding strategy appeared to have a larger impact on accuracy than the initial number of parents. Generally, maximum accuracies (in terms of the correlation between true and estimated breeding value) were consistently achieved under a mass selection strategy, pedigree method, and single seed descent method depending on the simulation parameters being tested. This study also investigated model updating, which involves retraining the prediction model with a new set of genotypes and phenotypes that have a closer relation to the population being tested. While it has been repeatedly shown that model updating generally improves prediction accuracy, it benefited some breeding strategies more than others. For low heritability traits (e.g., yield), conventional phenotype-based selection methods showed consistent rates of genetic gain, but genetic gain under genomic selection reached a plateau after fewer cycles. This plateauing is likely a cause of faster fixation of alleles and a diminishing of genetic variance when selections are made based on estimated breeding value as opposed to phenotype.

Bacterial brown spot (BBS) caused by Pseudomonas syringae pv. syringae (Pss), common bacterial blight (CBB) caused by Xanthomonas axonopodis pv. phaseoli (Xap) and Xanthomonas fuscans subsp. fuscans (Xff), and halo bacterial blight (HBB), caused by Pseudomonas syringae pv. phaseolicola (Psph), are major bacterial diseases that severely affect common bean yields and global food security. Andean-origin dry beans, representing large-seeded market classes, are particularly susceptible. Using 140,325 SNPs, a multi-locus GWAS was conducted on subsets of the Andean diversity panel (ADP) phenotyped for BBS in South Africa, CBB in Puerto Rico, South Africa, and Zambia, and HBB in South Africa, through natural infection, artificial inoculation, or both. Twenty-four QTL associated with resistance were identified: nine for BBS, eight for CBB, and seven for HBB. Four QTL intervals on Pv01, Pv03, Pv05, and Pv08 overlapped with BBS and HBB resistance. A genomic interval on Pv01, near the fin gene, which determines growth habit, was linked to resistance to all three pathogens. Different QTLs were detected for BBS and CBB resistance when phenotyped under natural infection versus artificial inoculation. These results underscore the importance of combining phenotyping methods in multi-GWAS to capture the full genetic spectrum. Previously recognized CBB resistance QTL SAP6 and SU91 and HBB resistance QTL HB4.2, and HB5.1, were observed. Other common (MAF >0.25) and rare (MAF <0.05) resistance QTL were also detected. Overall, these findings enhance the understanding and utilization of bacterial resistance present in ADP for the development of common beans with improved resistance.

Objectives: Reducing proanthocyanidin concentrations (inhibitors of iron absorption) in bean seed coats via alleles in the non-darkening (j gene) or slow darkening (Psd) gene will enhance iron (Fe) bioavailability across multiple market (color) classes of dry beans. Methods: Dry beans (Phaseolus vulgaris L.) with slow-darkening (SD), non-darkening (ND), and regular darkening (RD) traits were grown at research sites in North America (U.S. and Canada) and Africa (Zambia). The Caco-2 cell culture bioassay was used to determine the iron bioavailability of cooked beans. Mineral analysis was conducted by ICP-ES and phytate measured with a Megazyme™ kit. Flavonoids ( >25 compounds) were measured using a newly developed Acetone-Methanol (acidified) extraction methodology before analysis with UPLC/MS. Results: SD pinto beans from North Dakota provide 2-7x more bioavailable iron than RD pinto varieties. Iron and phytate concentrations were similar between SD and RD pinto beans, however, flavonoid analysis revealed 4x more proanthocyanidins were detected in RD pintos after cooking. Similar findings were demonstrated in ND yellow, cranberry and purple beans produced in North America and Africa. The absence or low levels of proanthocyanidins in the seed coats of ND beans correlated with 5-7x more bioavailable iron than RD beans. The greatest enhancement was observed in the yellow bean market class with a ND variety exhibiting 200% of a white kidney bean reference control. There was no relationship between iron bioavailability, phytate or iron concentrations in cooked beans. However, there was a strong (P < 0.001) association between iron bioavailability and proathocyanidins across all market classes. Conclusions: In addition to a brighter seed coat appearance after storage, this study reveals that downregulating the synthesis of proanthocyanidins with the slow darkening (Psd) or non-darkening (j) gene could be a novel, as well as a sustainable strategy to improve the iron bioavailability of dry beans, especially those susceptible to darkening, including yellow, pinto, purple and cranberry beans. Funding Sources: U.S. Department of Agriculture, Agricultural Research Service.

Flavonoids are secondary metabolites associated with plant seed coat and flower color. These compounds provide health benefits to humans as anti-inflammatory and antioxidant compounds. The expression of the late biosynthetic genes in the flavonoid pathway is controlled by a ternary MBW protein complex consisting of interfacing MYB, beta-helix-loop-helix (bHLH), and WD40 Repeat (WDR) proteins. P, the master regulator gene of the flavonoid expression in common bean (Phaseolus vulgaris L.), was recently determined to encode a bHLH protein. The T and Z genes control the distribution of color in bean seeds and flowers and have historically been considered regulators of the flavonoid gene expression. T and Z candidates were identified using reverse genetics based on genetic mapping, phylogenetic analysis, and mutant analysis. Domain and AlphaFold2 structure analyses determined that T encodes a seven-bladed β-propeller WDR protein, while Z encodes a R2R3 MYB protein. Deletions and SNPs in T and Z mutants, respectively, altered the 3D structure of these proteins. Modeling of the Z MYB/P bHLH/T WDR MBW complex identified interfacing sequence domains and motifs in all three genes that are conserved in dicots. One Z MYB motif is a possible beta-molecular recognition feature (β-MoRF) that only appears in a structured state when Z MYB is modeled as a component of a MBW complex. Complexes containing mutant T and Z proteins changed the interaction of members of the complex in ways that would alter their role in regulating the expression of genes in the flavonoid pathway.

Septoria nodorum blotch (SNB), caused by Parastagonospora nodorum, is a disease of durum and common wheat initiated by the recognition of pathogen-produced necrotrophic effectors (NEs) by specific wheat genes. The wheat gene Snn1 encodes a wall-associated kinase that directly interacts with the NE SnTox1 leading to the development of SNB. Here, sequence analysis of Snn1 from 114 accessions including diploid, tetraploid and hexaploid wheat species revealed that some wheat lines possess two copies of Snn1 (designated Snn1-B1 and Snn1-B2 ) approximately 120 kb apart. Snn1-B2 evolved relatively recently as a paralog of Snn1-B1 , and both genes have undergone diversifying selection. Three point mutations associated with the formation of the first SnTox1-sensitive Snn1-B1 allele from a primitive wild wheat were identified. Four subsequent and independent SNPs, three in Snn1-B1 and one in Snn1-B2 , converted the sensitive alleles to insensitive forms. Protein modeling indicated these four mutations could abolish Snn1 -SnTox1 compatibility either through destabilization of the Snn1 protein or direct disruption of the protein-protein interaction. High-throughput markers were developed for the causal mutations and evaluated on panels of durum and common wheat. The markers were able to correctly identify 96.9 % of SnTox1-sensitive durum wheat accessions, and a marker for the null allele was 100% accurate at predicting SnTox1-insensitive lines in both durum and spring wheat. Results of this study increase our understanding of the evolution, diversity, and function of Snn1-B1 and Snn1-B2 genes and will be useful for marker-assisted elimination of these genes for better host resistance.

Bean common mosaic virus (BCMV) and bean common mosaic necrosis virus (BCMNV) have a damaging impact on global common bean (Phaseolus vulgaris L.) cultivation, causing potential yield losses of over 80%. The primary strategy for controlling these viruses is through host plant resistance. This research aimed to identify and validate structural variations for the bc-ud gene as revealed by long-read sequencing, develop an efficient DNA marker to assist selection of bc-ud in snap and dry beans, and examine the interactions between the bc-ud allele and other BCMV resistance genes. A gene (Phvul.005G125100) model on chromosome Pv05, encoding a vacuolar protein-sorting 4 (Vps4) AAA+ ATPase endosomal sorting complexes required for transport (ESCRT) protein, was identified as the best candidate gene for bc-ud. An 84-bp repetitive insertion variant within the gene, exhibited 100% co-segregation with the bc-ud resistance allele across 264 common bean accessions. The 84-bp repetitive insertion was labeled with an indel marker IND_05_36225873 which was useful for tracking the bc-ud allele across diverse germplasm. A different single nucleotide polymorphism variant within the same candidate gene was associated with the bc-4 gene. Segregation in F2 populations confirmed bc-ud and bc-4 were alleles, so bc-4 was renamed bc-ur to fit gene nomenclature guidelines. The interactions of bc-ud and bc-ur with other resistance genes, such as bc-1 (receptor-like kinase on Pv03) and bc-2 (Vps4 AAA+ ATPase ESCRT protein on Pv11), validated gene combinations in the differential "host groups" effective against specific BCMV/BCMNV "pathogroups." These findings increase our understanding of the Bc-u locus, and enhance our ability to develop more resilient bean varieties through marker-assisted selection, reducing the impact of BCMV and BCMNV.

White mold (WM), caused by the ubiquitous fungus Sclerotinia sclerotiorum, is a devastating disease that limits production and quality of dry bean globally. In the present study, classic linkage mapping combined with QTL-seq were employed in two recombinant inbred line (RIL) populations, "Montrose"/I9365-25 (M25) and "Raven"/I9365-31 (R31), with the initial goal of fine-mapping QTL WM5.4 and WM7.5 that condition WM resistance. The RILs were phenotyped for WM reactions under greenhouse (straw test) and field environments. The general region of WM5.4 and WM7.5 were reconfirmed with both mapping strategies within each population. Combining the results from both mapping strategies, WM5.4 was delimited to a 22.60-36.25 Mb interval in the heterochromatic regions on Pv05, while WM7.5 was narrowed to a 0.83 Mb (3.99-4.82 Mb) region on the Pv07 chromosome. Furthermore, additional QTL WM2.2a (3.81-7.24 Mb), WM2.2b (11.18-17.37 Mb, heterochromatic region), and WM2.2c (23.33-25.94 Mb) were mapped to a narrowed genomic interval on Pv02 and WM4.2 in a 0.89 Mb physical interval at the distal end of Pv04 chromosome. Gene models encoding gibberellin 2-oxidase proteins regulating plant architecture are likely candidate genes associated with WM2.2a resistance. Nine gene models encoding a disease resistance protein (quinone reductase family protein and ATWRKY69) found within the WM5.4 QTL interval are putative candidate genes. Clusters of 13 and 5 copies of gene models encoding cysteine-rich receptor-like kinase and receptor-like protein kinase-related family proteins, respectively, are potential candidate genes associated with WM7.5 resistance and most likely trigger physiological resistance to WM. Acquired knowledge of the narrowed major QTL intervals, flanking markers, and candidate genes provides promising opportunities to develop functional molecular markers to implement marker-assisted selection for WM resistant dry bean cultivars.

White mold (WM) is a major disease in common bean (Phaseolus vulgaris L.), and its complex quantitative genetic control limits the development of WM resistant cultivars. WM2.2, one of the nine meta-QTL with a major effect on WM tolerance, explains up to 35% of the phenotypic variation and was previously mapped to a large genomic interval on Pv02. Our objective was to narrow the interval of this QTL using combined approach of classic QTL mapping and QTL-based bulk segregant analysis (BSA), and confirming those results with Khufu de novo QTL-seq. The phenotypic and genotypic data from two RIL populations, ‘Raven’/I9365-31 (R31) and ‘AN–37’/PS02–029C–20 (Z0726-9), were used to select resistant and susceptible lines to generate subpopulations for bulk DNA sequencing. The QTL physical interval was determined by considering overlapping interval of the identified QTL or peak region in both populations by three independent QTL mapping analyses. Our findings revealed that meta-QTL WM2.2 consists of three regions, WM2.2a (4.27-5.76 Mb; euchromatic), WM 2.2b (12.19 to 17.61 Mb; heterochromatic), and WM2.2c (23.01-25.74 Mb; heterochromatic) found in both populations. Gene models encoding for gibberellin 2-oxidase 8, pentatricopeptide repeat, and heat-shock proteins are the likely candidate genes associated with WM2.2a resistance. A TIR-NBS-LRR class of disease resistance protein (Phvul.002G09200) and LRR domain containing family proteins are potential candidate genes associated with WM2.2b resistance. Nine gene models encoding disease resistance protein [pathogenesis-related thaumatin superfamily protein and disease resistance-responsive (dirigent-like protein) family protein etc] found within the WM2.2c QTL interval are putative candidate genes. WM2.2a region is most likely associated with avoidance mechanisms while WM2.2b and WM2.2c regions trigger physiological resistance based on putative candidate genes.

KEY MESSAGE:A reference study for breeders aiming at maximizing genetic gain in common bean. Depending on trait heritability and genetic architecture, conventional approaches may provide an advantage over other frameworks. Dry beans (Phaseolus vulgaris L.) are a nutrient dense legume that is consumed by developed and developing nations around the world. The progress to improve this crop has been quite steady. However, with the continued rise in global populations, there are demands to expedite genetic gains. Plant breeders have been at the forefront at increasing yields in the common bean. As breeding programs are both time-consuming and resource intensive, resource allocation must be carefully considered. To assist plant breeders, computer simulations can provide useful information that may then be applied to the real world. This study evaluated multiple breeding scenarios in the common bean and involved five selection strategies, three breeding frameworks, and four different parental population sizes. In addition, the breeding scenarios were implemented in three different traits: days to flowering, white mold tolerance, and seed yield. Results from the study reflect the complexity of breeding programs, with the optimal breeding scenario varying based on trait being selected. Relative genetic gains per cycle of up to 8.69% for seed yield could be obtained under the use of the optimal breeding scenario. Principal component analyses revealed similarity between strategies, where single seed descent and the modified pedigree method would often aggregate. As well, clusters in the direction of the Hamming distance eigenvector are a good indicator of poor performance in a strategy.