RT Dissertation/Thesis T1 Inheritance of Barley yellow dwarf virus resistance in maize A1 Horn,Frederike WP 2015/11/19 AB Barley yellow dwarf (BYD) is one of the economically most important virus diseases in cereals. Due to increasing winter temperatures it is expected that BYD will become an increasing problem in maize cultivation. In earlier studies, it was reported that BYD has a negative impact on plant performance of maize. BYD virus (BYDV) is transmitted by aphids and the best control of the virus is the development of resistant maize cultivars. Therefore, the first objectives of my thesis research were to (i) determine phenotypic and genotypic variation in five segregating populations and in a broad germplasm set of maize with respect to BYDV tolerance and resistance as well as to (ii) quantify the influence of BYDV infection on the plant traits plant height, ear height, and flowering time. I observed a negative impact of BYDV infection on maize plant traits which shows that the development of resistant maize cultivars is of high importance for maize cultivation. Furthermore, in the connected biparental populations as well as in the association mapping population, I observed a high genotypic variance with regard to BYDV resistance which is the requirement for successful breeding and the identification of genome regions which contribute to BYDV resistance. The evaluation of BYDV resistance by the inoculation with BYDV and by double antibody sandwich enzyme-linked immunosorbent assay (DASELISA) is dificult to be included in the breeding process. Therefore, molecular markers are of high importance for the improvement of BYDV resistance by breeding. Therefore, the objective of this study was the (iii) identification of genome regions which are involved in the BYDV resistance by a genome wide association study (GWAS). For the BYDV resistance traits, significantly (α=0.01) associated SNPs were identified in the GWAS on chromosome 10 and 4. The SNPs identified for virus extinction on chromosome 10 explained in a simultaneous fit 25% of the phenotypic variance and were located in gene regions which were in other plants described to be involved in resistance mechanisms. This suggests that BYDV resistance is inherited oligogenically and that genes involved in general resistance mechanisms are also involved in BYDV resistance in maize. GWAS has the advantage that a large number of alleles per locus can be surveyed simultaneously, and because historical recombinations can be used, the mapping resolution is higher compared to classical linkage mapping. Nevertheless, genes contributing to phenotypic variation which show a low allele frequency can remain undetected. Due to a balanced allele frequency in segregating populations, linkage mapping has the advantage of higher QTL detection power compared to GWAS. Therefore, the objective of this study was to (iv) validate the genome regions with a linkage analysis in connected biparental crosses. The genome region on chromosome 10 which was identified in the GWAS to be linked to BYDV resistance could be validated in the linkage mapping study with connected populations as well as in the single populations. Furthermore, the QTL on chromosome 10 colocalized with the QTL identified in controlled greenhouse conditions. In earlier studies, QTL for other virus resistances were identified on chromosome 10. This suggests that these genes are involved in multiple virus resistances. The identified genome regions explain 45% of the phenotypic variance and are, therefore, promising for the use in MAS. The broad genotypic variation with regard to BYDV resistance, observed in my thesis research, provided a good basis for the successful identification of molecular markers which are associated with BYDV resistance in maize. The markers identified in my study by GWAS were validated by a linkage mapping approach and are promising for the use in marker assisted selection on BYDV resistance in maize breeding. K1 Gerstengelbverzwergungsvirus K1 Mais K1 QTL PP Hohenheim PB Kommunikations-, Informations- und Medienzentrum der Universität Hohenheim UL http://opus.uni-hohenheim.de/volltexte/2015/1126