Fine mapping of an anthracnose-resistance locus in Andean common bean cultivar Amendoim Cavalo

Authors: GILIO, THIAGO - Universidade Estadual De Maringá; Hurtado-Gonzales, Oscar; GONCALVES-VIDIGAL, MARIA - Universidade Estadual De Maringá; VALENTINI, GISELI - Universidade Estadual De Maringá; FERREIRA ELIAS, JULIO - Universidade Estadual De Maringá; Song, Qijian; Pastor Corrales, Marcial - Talo

Submitted to: PLOS ONE
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/12/2020
Publication Date: 10/7/2020
Citation: Gilio, T., Hurtado-Gonzales, O.P., Goncalves-Vidigal, M.C., Valentini, G., Ferreira Elias, J.C., Song, Q., Pastor Corrales, M.A. 2020. Fine mapping of an anthracnose-resistance locus in Andean common bean cultivar Amendoim Cavalo. PLOS ONE. 15(10):0239763. https://doi.org/10.1371/journal.pone.0239763.
DOI: https://doi.org/10.1371/journal.pone.0239763

Interpretive Summary: Anthracnose is a very destructive disease of common bean in the United States, Latin America, and Africa. We are conducting genetic research aiming to find new genes conferring broad-spectrum resistance to the highly variable anthracnose pathogen. One objective is to find resistance genes in large-seeded bean varieties that are originally from the Andean highlands of South America. Genes of Andean origin often confer very effective resistance to the strains of the pathogen that infect small and medium-seeded varieties that are originally from Mexico and Meso-America. These are the varieties that are grown in Brazil, Argentina, Central America, Mexico, and the United States. We first identified a new anthracnose resistance gene present in the Andean bean Amendoim Cavalo. This gene conferred broad-resistance to highly virulent Meso-American strains of the anthracnose pathogen. We then combined traditional and modern genetic and DNA tools to study the new resistance gene. The results revealed the position of the new gene in a very small DNA region and we identified DNA sequence markers near the new resistance gene. These markers can be used for following the Andean resistance gene as it gets bred into Meso-American beans. These results will valuable to scientists in private industry, in the government, or in universities developing Meso-American common beans with resistance to anthracnose.

Technical Abstract: Anthracnose, caused by the fungal pathogen Colletotrichum lindemuthianum, is one of the world's most destructive diseases of common bean. The use of resistant cultivars is the most cost effective strategy to manage this disease; however, durable resistance is difficult to achieve due to the vast virulence diversity of the anthracnose pathogen. Finding new genes with broad spectrum resistance increases the prospect of designing an effective anthracnose-management strategy. The phenotyping of the Andean landrace Amendoim Cavalo (AC) with 15 highly diverse Mesoamerican and Andean races of C. lindemuthianum revealed the broad-spectrum resistance of AC and specifically its resistance to highly virulent Mesoamerican races. Genetic analysis uncovered the presence of a single and dominant anthracnose resistance locus in AC that we are calling provisionally Co-AC. Bulk segregant analysis and genetic mapping of the F2 populations determined the position of the Co-AC locus on a 631 Kbp genomic region flanked by SNP markers SS56 and SS92 on the lower arm of chromosome Pv01. Using these two markers to screen 660 F3 plants from 57 F2:3 families enabled the identification of 77 F3 plants with unique recombinant events. We then used these plants to fine mapping of the Co-AC locus with nine additional markers that positioned the Co-AC locus in a significantly smaller genomic region (9.4 Kbp) flanked by SNP markers SS102 and SS165. In addition, the common bean reference genome revealed three candidate genes in this genomic region. This study corroborated the broad-spectrum of AC to C. lindemuthianum and revealed the occurrence of the Co-AC locus. Fine mapping positioned this locus on a small genomic region on the lower end of chromosome Pv01 that contained three candidate genes for AC.