PMC:4502374 / 36144-37919 JSONTXT

{"project":"2_test","denotations":[{"id":"25943521-7851788-43367142","span":{"begin":562,"end":566},"obj":"7851788"},{"id":"25943521-8770605-43367143","span":{"begin":589,"end":593},"obj":"8770605"}],"text":"Here, by the use of detached leaf assays, different phenotypes of disease resistance were observed. Some progenies developed no lesions. In others, lesions appeared and then necrotic tissue developed around them in a way that resembled a hypersensitive reaction. These lesions did not sporulate. Furthermore, delayed incubation period also was observed. This finding suggests multiple resistance mechanisms and genes involved in resistance. In total, we detected 13 QTL with LOD scores above the limits established by the permutation tests (Churchill and Doerge 1994; Doerge and Churchill 1996), which ranged from 2.5 to 3.2. All alleles that confer resistance were derived from the resistant parent A. magna. They confer less and smaller lesions, lesions with less sporulation, and longer disease incubation period. Although multiple QTL were detected, one particular marker locus (Ah-280) located on LGB08 is linked to QTL associated to all the four components of rust resistance evaluated in both years. The differences between the average phenotypes of RILs that harbor the A. magna allele of this marker compared with those that harbor the A. ipaënsis one are striking (Figure 4). The effect of A. magna alleles on incubation period appear less pronounced. However, this is attributable to the fact that this can only be measured on a subset of genotypes: the minority that shows symptoms. Because resistant genotypes do not have an incubation period, it is not possible to measure with precision the allelic effect on this trait of the whole range of genotypes. This fact could also explains the high estimates of the proportion of phenotypic variance explained by the QTL detected, which tend to be inflated by the small number of progenies with that particular trait."}