BackgroundThe Andean cultivar Paloma is resistant to Mesoamerican and Andean races of Colletotrichum lindemuthianum, the fungal pathogen that causes the destructive anthracnose disease in common bean. Remarkably, Paloma is resistant to Mesoamerican races 2047 and 3481, which are among the most virulent races of the anthracnose pathogen. Most genes conferring anthracnose resistance in common bean are overcome by these races. The genetic mapping and the relationship between the resistant Co-Pa gene of Paloma and previously characterized anthracnose resistance genes can be a great contribution for breeding programs.ResultsThe inheritance of resistance studies for Paloma was performed in F2 population from the cross Paloma (resistant) × Cornell 49–242 (susceptible) inoculated with race 2047, and in F2 and F2:3 generations from the cross Paloma (resistant) × PI 207262 (susceptible) inoculated with race 3481. The results of these studies demonstrated that a single dominant gene confers the resistance in Paloma. Allelism tests performed with multiple races of C. lindemuthianum showed that the resistance gene in Paloma, provisionally named Co-Pa, is independent from the anthracnose resistance genes Co-1, Co-2, Co-3, Co-4, Co-5, Co-6, Co-12, Co-13, Co-14, Co-15 and Co-16. Bulk segregant analysis using the SNP chip BARCBean6K_3 positioned the approximate location of Co-Pa in the lower arm of chromosome Pv01. Further mapping analysis located the Co-Pa gene at a 390 kb region of Pv01 flanked by SNP markers SS82 and SS83 at a distance of 1.3 and 2.1 cM, respectively.ConclusionsThe results presented here showed that Paloma cultivar has a new dominant gene conferring resistance to anthracnose, which is independent from those genes previously described. The linkage between the Co-Pa gene and the SS82 and SS83 SNP markers will be extremely important for marker-assisted introgression of the gene into elite cultivars in order to enhance resistance.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-017-3685-7) contains supplementary material, which is available to authorized users.

Anthracnose (ANT) and angular leaf spot (ALS) caused by Colletotrichum lindemuthianum and Pseudocercospora griseola, respectively, are devastating diseases of common bean around the world. Therefore, breeders are constantly searching for new genes with broadspectrum resistance against ANT and ALS. This study aimed to characterize the genetic resistance of California Dark Red Kidney (CDRK) to C. lindemuthianum races 73, 2047, and 3481 and P. griseola race 63-39 through inheritance, allelism testing, and molecular analyses. Genetic analysis of response to ANT and ALS in recombinant inbred lines (RILs) from a CDRK × Yolano cross (CY) showed that the resistance of CDRK cultivar is conferred by a single dominant loci, which we named CoPv01 CDRK /PhgPv01 CDRK. Allelism tests performed with race 3481showed that the resistance gene in CDRK is independent of the Co-1 and Co-AC. We conducted co-segregation analysis in genotypes of 110 CY RILs and phenotypes of the RILs in response to different races of the ANT and ALS pathogens. The results revealed that CoPv01 CDRK and PhgPv01 CDRK are coinherited, conferring resistance to all races. Genetic mapping of the CY population placed the CoPv01 CDRK /PhgPv01 CDRK loci in a 245 Kb genomic region at the end of Pv01. By genotyping 19 RILs from the CY population using three additional markers, we fine-mapped the CoPv01 CDRK /PhgPv01 CDRK loci to a smaller genomic region of 33 Kb. This 33 Kb region harbors five predicted genes based on the common bean reference genome. These results can be applied in breeding programs to develop bean cultivars with ANT and ALS resistance using marker-assisted selection.

Anthracnose (ANT) and angular leaf spot (ALS) are devastating diseases of common bean (Phaseolus vulgaris L.) worldwide, and identification of new sources of ANT and ALS resistance is a major priority in breeding programs. The ANT and ALS reaction of 57 Andean and 58 Mesoamerican accessions from five Brazilian states were evaluated. Three Mesoamerican and eight Andean accessions were resistant to races 9, 65, 73, 2047, and 3481 of the ANT pathogen, while four Mesoamerican and 14 Andean accessions were resistant to four of the ANT pathogen races. Furthermore, 13 Mesoamerican and 30 Andean accessions were resistant to races 31‐23 and 63‐39 of the ALS pathogen. To understand the genetic basis of ANT and ALS resistance, a genome‐wide association study (GWAS) was conducted using the 115 accessions, revealing new sources of resistance in Andean and Mesoamerican accessions. The single nucleotide polymorphism (SNP) markers associated with races 9 and 73 of ANT was positioned on chromosome Pv04; resistance to race 65 on chromosomes Pv01, Pv04, and Pv08; and resistance to races 2047 and 3481 on chromosomes Pv10 and Pv05, respectively. Furthermore, SNPs associated with race 31‐23 of Pseudocercospora griseola (Sacc.) Crous & U. Braun were mapped on chromosomes Pv02 and Pv04, whereas for race 63‐39, SNPs were mapped on chromosomes Pv03, Pv06, and Pv08. The SNP markers and candidate genes found associated with the resistance should be validated in segregating populations, which could further be used for marker‐assisted selection. As a result, breeding programs might be able to develop resistant bean cultivars to ANT and ALS.

RESUMOPalavras-chave adicionais: Epidemiologia, Manejo integrado, Melhoramento genético.A ferrugem alaranjada é atualmente uma das principais doenças da cana-de-açúcar. Redução na produtividade de genótipos suscetíveis e intermediários superiores a 40% foram registradas em muitos países, inclusive no Brasil. Este trabalho foi desenvolvido com o objetivo de monitorar os principais genótipos de cana-de-açúcar plantados no Brasil, sob alta pressão de inóculo, quanto à ocorrência e ao desenvolvimento da ferrugem alaranjada. O experimento foi conduzido em área experimental da Usina Univalem, do Grupo Raízen S.A., localizada em Valparaíso (SP). O delineamento experimental utilizado foi em blocos casualizados, com 38 tratamentos (genótipos) e quatro repetições. Cada parcela foi constituída por três linhas de cinco metros, espaçadas de 1,4m. Entre cada parcela foi incluída uma linha do genótipo CV14, suscetível à ferrugem alaranjada. A partir da emergência Araújo, K.L.; Canteri, M.G.; Gilio, T.A.S.; Neubauer, R.A.; Sanches, P.B.; Sumida, C.H.; Giglioti, E.A. Resistência genotípica e monitoramento da favorabilidade para ocorrência da ferrugem alaranjada da cana-de-açúcar. Summa Phytopathologica, v.39, n.4, p.271-275, 2013. das plantas, todas as parcelas foram monitoradas mensalmente para determinar o início do aparecimento dos sintomas da doença. Depois de constatados os primeiros sintomas, a severidade da ferrugem alaranjada foi quantificada mensalmente na folha +3 em três plantas por parcela. Os meses mais favoráveis para ocorrência da doença foram Fevereiro, Março, Abril e Maio. Foram observados sintomas da ferrugem alaranjada nos genótipos CTC 9, CV 14, RB93-5641, SP84-2025, RB72-454, SP89-1115, SP81-3250, RB85-5156, CTC 15, RB92-579, SP83-2847 e RB92-5211. Os genótipos SP84-2025 e CV 14 foram os mais suscetíveis à doença. Este trabalho contribui para aperfeiçoar o manejo integrado da ferrugem alaranjada no Brasil, além de auxiliar os programas de melhoramento visando à obtenção de novas variedades resistentes à doença.Currently, orange rust is one of the major diseases affecting sugar cane. Yield losses above 40% have been recorded for susceptible and intermediate genotypes in different countries, including Brazil. This study was developed with the aim of monitoring the major sugar cane genotypes grown in Brazil under high inoculum pressure for the occurrence and the development of orange rust. The experiment was conducted in an experimental field of Univalem Plant, Group "Raizen S.A.", located in Valparaiso (São Paulo State). The adopted experimental design was in randomized blocks with 38 treatments (genotypes) and four replicates. Each plot consisted of three lines of five meters, spaced 1.4 m apart. A line of genotype CV14, susceptible to orange rust, was included between each plot. From plant emergence, Araújo, K.L.; Canteri, M.G.; Gilio, T.A.S.; Neubauer, R.A.; Sanches, P.B.; Sumida, C.H.; Giglioti, E.A. Genotypic resistance and monitoring of favorability for the occurrence of orange rust in sugarcane. Summ...

Bean rust, caused by Uromyces appendiculatus, is a devastating disease of common bean (Phaseolus vulgaris) in the Americas and Africa. The historically important Ur-3 gene confers resistance to many races of the highly variable bean rust pathogen that overcome other rust resistance genes. Existing molecular markers tagging Ur-3 for use in marker-assisted selection produce false results. Here, we describe the fine mapping of the Ur-3 locus for the development of highly accurate markers linked to Ur-3. An F2 population from the cross Pinto 114 (susceptible) × Aurora (resistant with Ur-3) was evaluated for its reaction to four different races of U. appendiculatus. A bulked segregant analysis using the SNP chip BARCBEAN6K_3 placed the approximate location of Ur-3 in the lower arm of chromosome Pv11. Specific SSR and SNP markers and haplotype analysis of 18 sequenced bean varieties positioned Ur-3 in a 46.5 kb genomic region from 46.96 to 47.01 Mb on Pv11. We discovered in this region the SS68 KASP marker that was tightly linked to Ur-3. Validation of SS68 on a panel of 130 diverse common bean cultivars containing all known rust resistance genes revealed that SS68 was highly accurate and produced no false results. The SS68 marker will be of great value in pyramiding Ur-3 with other rust resistance genes. It will also significantly reduce time and labor associated with the current phenotypic detection of Ur-3. This is the first utilization of fine mapping to discover markers linked to rust resistance in common bean.

63Bean rust is a devastating disease of common bean in the Americas and Africa. The historically 64 important Ur-3 gene confers resistance to many races of the highly variable bean rust pathogen 65 that overcome all known rust resistance genes. Existing molecular markers tagging Ur-3 for use 66 in marker assisted selection produce false results. We described here the fine mapping of Ur-3 67 for the development of highly accurate markers linked to this gene. An F 2 population from Pinto 68 114 × Aurora was evaluated for its reaction to four different races of the bean rust pathogen. A 69 bulked segregant analysis using the SNP chip BARCBEAN6K_3 positioned the approximate 70 location of the Ur-3 locus to the lower arm of chromosome Pv11. Specific SSR and SNP 71 markers and haplotype analysis of 18 sequenced bean lines led to position the Ur-3 locus to a 72 46.5 Kb genomic region. We discovered a KASP marker, SS68 that was tightly linked to the Ur-73 3 locus. Validation of SS68 on a panel of 130 diverse common bean lines and varieties 74 containing all known rust resistance genes revealed that it was highly accurate producing no false 75 results. The SS68 marker will be of great value to pyramid Ur-3 with other rust resistance genes. 76It will also reduce significantly time and labor associated with the current phenotypic detection 77 of Ur-3. This is the first utilization of fine mapping to discover markers linked to a rust 78 resistance in common bean.

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. Genetic analysis confirmed the presence of a single, dominant anthracnose-resistance locus in AC, which we provisionally named Co-AC. Bulk segregant analysis and genetic mapping of two F 2 populations from the crosses AC × PI207262 and AC × G 2333 were used to determine the position of the Co-AC locus in a 631 Kbp genomic region flanked by the SNP markers SS56 and SS92 on the lower arm of chromosome Pv01. By genotyping 77 F 3 plants from the AC × PI207262 cross using nine additional markers, we fine-mapped the Co-AC locus to a significantly smaller genomic region (9.4 Kbp) flanked by the SNP markers SS102 and SS165. This 9.4 Kbp region harbors three predicted genes based on the common bean reference genome, notably including the gene model Phvul.001G244300, which encodes Clathrin heavy chain 1, a protein that supports specific stomatal regulation functions and might play a role in plant defense signaling. Because the Co-AC resistance locus is linked in cis, it can be selected with great efficiency using molecular markers. These results will be very useful for breeding programs aimed at developing bean cultivars with anthracnose resistance using marker-assisted selection. This study revealed the broad-spectrum resistance of AC to C. lindemuthianum and the existence of the Co-AC anthracnose-resistance locus. Fine mapping positioned this locus in a small genomic region on the lower end of chromosome Pv01 that contained three candidate genes for the Co-AC locus.

This work was carried out with the objective of performing a molecular and aggressiveness characterization of F. solani and F. oxysporum f.sp. passiflorae collected in the Pantanal, Cerrado and Amazon biomes. We selected the most aggressive isolates for use in breeding programs aiming resistance to Collar Rot and Fusariosis. For inoculation of the isolates of F. oxysporum f.sp. passiflorae the washed root method was used. The molecular characterization of the isolates was carried out by partial sequencing of the Transcribed Internal Spacer of the rDNA region. The isolates of F. solani formed two distinct groups in relation to aggressiveness. Among all isolates, FSUNEMAT 40 and FSUNEMAT 46 were the most aggressive. The model with K=2 was taken as the best model to explain the genetic structure of the F. solani populations, with clear combinations of genes from both gene pools. There were three groups with respect to the aggressiveness of the isolates of F. oxysporum f.sp. passiflorae, with the isolated FOUNEMAT 22 being the most aggressive. In view of these results, the isolates of F. solani collected in P. edulis in the state of Mato Grosso presented a high molecular variability independent from the biome of origin, and this was also observed in the tests of aggressiveness. The results indicate the need to consider the molecular variability and the aggressiveness of the pathogens in the evaluation of genotypes of sour passion fruit in programs of selection of resistant cultivars.