Inheritance of quantitative resistance and aggressiveness in the wheat/Fusarium pathosystem with emphasis on Rht dwarfing genes

Fusarium head blight (FHB), or scab, is one of the most devastating fungal diseases affecting small-grain cereals and maize, causing severe yield losses and contamination of grain with mycotoxins such as deoxynivalenol (DON) worldwide. Fusarium graminearum (teleomorph Gibberella zeae) and Fusarium culmorum are the most prevalent Fusarium species in wheat production in Central and Northern Europe. Breeding for increased resistance to FHB in wheat is considered the most effective strategy for large scale disease management and mycotoxin reduction. Height reducing Rht genes are extensively used in wheat breeding programmes worldwide in order to improve lodging resistance and yield potential, with Rht-D1b being the most important Rht allele in Northern Europe. However, their individual effects on FHB resistance are yet unclear. Due to the incremental approach to increase host resistance the question arises whether the Fusarium pathogen has the capability to adapt by increased aggressiveness and/or increased mycotoxin production.\nTherefore, the objectives of the present study were to investigate the effects on FHB resistance of Rht-D1b and additional Rht alleles, the segregation variance for FHB resistance and identification of FHB resistance QTL in subsequent mapping analyses in three crossing populations segregating for the semi-dwarfing Rht-D1b allele and two sets of isogenic wheat lines. Regarding the pathogen, the study aims to determine the segregation variance in two F. graminearum crosses of highly aggressive parental isolates and to examine the stability of host FHB resistance, pathogen aggressiveness and the complex host-pathogen-environment interactions in a factorial field trial. All experiments were conducted on the basis of multienvironmental field trials including artificial inoculation of spores. \nThe presence of Rht-D1b resulted in 7-18% reduction in plant height, but considerably increased FHB severity by 22-53% within progenies from three tested European elite winter wheat crosses. In the following QTL mapping analyses the QTL with the strongest additive effects was located at the Rht-D1 locus on chromosome arm 4DS and accordingly coincided with a major QTL for plant height in all three wheat populations. On total, a high number of 8 to 14 minor QTL for FHB reaction that were found in the three populations which emphasised the quantitative inheritance of FHB resistance in European winter wheat. The detected QTL mostly showed significant QTL-by-environment interactions and often coincided with QTL for plant height. By means of isogenic lines in the genetic background of the variety Mercia, Rht-D1b and Rht-B1d significantly increased mean FHB severity by 52 and 35%, respectively, compared to the wild-type (rht). Among the Maris Huntsman data set, the Rht alleles increased mean FHB severity by 22 up to 83%, but only the very short lines carrying Rht-B1c or Rht-B1b+Rht-D1b showed significance. \nThe analyses of 120 progenies of the crosses from each of the highly aggressive parental F. graminearum isolates revealed significant genetic variation for aggressiveness, DON and fungal mycelium production following sexual recombination. This variation resulted in stable transgressive segregants towards increased aggressiveness in one of the two progeny. The factorial field trial, including eleven F. graminearum and F. culmorum isolates varying in aggressiveness and seven European elite winter wheat varieties, varying in their FHB resistance level, displayed no significant wheat variety × isolate interaction. Nevertheless, isolates possessing increased aggressiveness significantly increased FHB severity and DON production at a progressive rate on varieties with reduced FHB resistance.\nIn conclusion, the analysed Rht alleles led to differently pronounced negative effects on FHB resistance that strongly depended on the genetic background. However, significant genetic variation for FHB resistance exists for selection and, thus, to largely counteract these effects by accumulating major and minor FHB resistance QTL. Significant genetic variation for aggressiveness among F. graminearum and the capability to increase its level of aggressiveness beyond yet known levels simply by sexual recombination may lead to long term erosion of FHB resistance. The rate at which increased aggressiveness develops will depend on the selection intensity and whether it is of constant, episodic or balanced nature. Consequently, the selection pressure imposed on the pathogen should be minimized by creating and maintaining a broad genetic base of FHB resistance that relies on more than one genetically unrelated resistance source by combining phenotypic and marker-assisted selection to achieve a sustainably improved FHB resistance in wheat breeding.