Pyramidisierung von QTL im Hinblick auf eine Verbesserung der <em>Barley yellow dwarf virus</em> Toleranz der Gerste und genetische Analyse der Toleranz gegenüber <em>Wheat dwarf virus</em>

Abstract

Barley yellow dwarf virus (BYDV) and Wheat dwarf virus (WDV) are economically important pathogens of barley which may become even more important due to global warming. In barley several loci conferring tolerance to BYDV are known, e. g. Ryd2, Ryd3 and a QTL (quantitative trait locus) on chromosome 2H. One aim of the present study was to get information whether the level of tolerance against BYDV in barley can be improved by combining these loci. Another objective was to analyse the tolerance of the cultivar 'Post' to WDV. For combining the above mentioned tolerance loci against BYDV a winter and a spring barley population of doubled haploid (DH) lines was genotyped by molecular markers for the presence of the susceptibility or the resistance encoding allele at respective loci (Ryd2, Ryd3, QTL on chromosome 2H) and were tested for their level of BYDV-tolerance after inoculation with viruliferous (BYDV-PAV) aphids in two-years field trials at four locations. In DH-lines carrying the combination Ryd2 and Ryd3 a significant reduction of the virus titre and a much lower infection rate were detected compared to lines carrying only one or none of these genes. Furthermore, spring barley DH-lines with this allele combination also showed a significantly higher relative grain yield compared to lines carrying only Ryd2 or Ryd3. Overall these results show that the combination of Ryd2 and Ryd3 leads to quantitative resistance against BYDV-PAV. For analysis of the tolerance to WDV detected in the cultivar 'Post' two DH-line populations of the cross 'Post' (tolerant) x 'Vixen'  (susceptible) were phenotyped in field trails after inoculation with WDV carrying leafhoppers (Psammotettix alienus). QTL were detected on chromosome 1H, 2H, 3H and 4H. The most important one is the QTL for symptom score and relative plant height on chromosome 4H, which was detected at the position of the SSR-marker HVM3 in both populations and explained up to 32 % of the phenotypic variance.