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Use of non‐adapted quantitative trait loci for increasing Fusarium head blight resistance for breeding semi‐dwarf wheat
Author(s) -
Miedaner Thomas,
Herter Cathérine P.,
Ebmeyer Erhard,
Kollers Sonja,
Korzun Viktor
Publication year - 2019
Publication title -
plant breeding
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.583
H-Index - 71
eISSN - 1439-0523
pISSN - 0179-9541
DOI - 10.1111/pbr.12683
Subject(s) - dwarfing , biology , quantitative trait locus , fusarium , doubled haploidy , allele , population , cultivar , fusarium culmorum , introgression , agronomy , veterinary medicine , genetics , gene , demography , medicine , sociology
Semi‐dwarf wheat is an important prerequisite for releasing a successful commercial cultivar in high‐yielding environments. In Northern Europe, this aim is achieved by using one of the dwarfing genes Rht‐B1 (formerly known as Rht‐1 ) or Rht‐D1 ( Rht‐2 ). Both genes, however, result in a higher susceptibility to Fusarium head blight (FHB). We analysed the possibility to use the two non‐adapted FHB resistance quantitative trait loci Fhb1 and Fhb5 (syn. QFhs.ifa‐5A ) to counterbalance the negative effect of the dwarfing allele Rht‐D1b in a winter wheat population of 585 doubled‐haploid (DH) lines segregating for the three loci. All lines were inoculated with Fusarium culmorum at four locations and analysed for FHB severity, plant height, and heading date. The DH population showed a significant ( p < 0.001) genotypic variation for FHB severity ranging from 3.6% to 65.9% with a very high entry‐mean heritability of 0.95. The dwarfing allele Rht‐D1b reduced plant height by 24 cm, but nearly doubled the FHB susceptibility (24.74% vs. 12.74%). The resistance alleles of Fhb1 and Fhb5 reduced FHB susceptibility by 6.5 and 11.3 percentage points, respectively. Taken all three loci together, Fhb5 alone was already able to reduce FHB susceptibility to the same extent as Rht‐D1b increased it. This opens new avenues for selecting semi‐dwarf wheat by marker‐assisted introgression of Fhb5 without the enhancement of FHB susceptibility.