Genetic linkage map of Phaseolus vulgaris and identification of QTLs responsible for resistance to Xanthomonas axonopodis pv. phaseoli

Abstract

Common bean (Phaseolus vulgaris) cultivars with a high degree of resistance to Xanthomonas axonopodis pv. phaseoli (Xap) are not available in Brazil. Despite many studies, a low degree of resistance to Xap continues to exist due to its complex genetic inheritance, which is not well known. The objectives of this research were to complement a common bean genetic map based on the cross between a susceptible genotype 'HAB-52' and a resistant genotype 'BAC-6', and to map and analyze genomic regions (quantitative trait loci – QTLs) related to Xap resistance. Eleven linkage groups were determined using 143 RAPD markers, covering 1,234.5 cM of the genome. This map was used to detect QTLs associated with Xap resistance on leaves and pods. The averages of disease severity on leaves (represented by the transformed disease index – TDI) and pods (represented by the diameter of lesion on pods – DLP) were added to the data of the linkage map. Five TDI QTLs and only one LDP QTL were detected. The TDI QTLs were placed in the A, B, G and J linkage groups, with phenotypic variations ranging from 12.7 to 71.6%. The DLP QTL explained 12.9% of the phenotypic variation and was mapped in a distinct linkage group. These results indicate that there are different genes involved in the control of resistance on leaves and pods.

Critical disease components of common bacterial blight to effectively evaluate resistant genotypes of snap bean

“…This result is expected due to the type of evaluation and the period in which resistance was assessed on pods, the more advanced ontogenic stage of pod formation. These estimates of low linear correlation values between DL and the other components of resistance also agree with previous studies on the complex heritage for pod resistance to CBB, which showed that the genes that control resistance on leaves of the snap beans are not the same that control resistance on pods (Arnaud-Santana et al 1994;Rodrigues et al 1999;Santos et al 2003).…”

“…phaseoli, as expressed by molecular biology data and by reactions observed after inoculation of differential hosts with the same isolate (Mahuku et al 2006;Márquez et al 2007;Mkandawire et al 2004). While investigating regions of the bean plant genome related to CBB resistance, Santos et al (2003) observed that the genes that confer resistance to Xap on leaves differ from those that confer resistance on pods.…”

“…More than 20 QTL (quantitative trait loci) related to CBB resistance are known, with variable genetic effects distributed across all of the 11 bean plant chromosomes (Asensio-S-Manzanera et al 2005;Kelly et al 2003;Santos et al 2003). The statistical similarity between these accessions of snap bean and the accessions of common Table 3 Spearman's correlations between three components of disease resistance of snap bean and common bean against common bacterial blight caused by isolates 1394-98 (E1) and 775-90 (E2) of Xanthomonas axonopodis pv.…”

Reaction of common bean lines to Xanthomonas axonopodis pv. phaseoli and Curtobacterium flaccumfaciens pv. Flaccumfaciens

“…Six QTLs in F 3 plants resulting from the BAC-6 and HAB-52 cross were identified by Santos et al (2003). Five of these QTLs were associated with resistance of leaves and one of pods, with a phenotypic variation from 12.7 to 68.7% for leaf and 12.9% for pod resistance.…”

“…These pathogens are widespread in the producing regions, causing yield losses, especially when stimulated by favorable environmental conditions such as high temperatures (Theodoro 2004) The first pathogen symptoms of common bacterial blight appear on the shoot, consisting primarily of small watersoaked areas in the leaves, evolving to necrosis and imperfections in the seeds such as discoloration of the hilum, yellow spots, and wrinkling of the seed coat, which can reduce yields by 10 to 70% (Diaz et al 2001, Bianchini et al 2005. The inheritance of resistance to this pathogen is genetically complex, described by several authors as oligogenic or polygenic (Kelly et al 2003, Santos et al 2003, Manzanera et al 2005. According to Zapata et al (2010), Ferreira and Grattapaglia (2003), and Marquez et al (2007), the number of genes, degrees and interactions involved in the expression of this trait may vary.…”