Barley and Wheat Resistance Genes for Fusarium Head Blight

Abstract

The genetic control of resistance to Fusarium head blight (FHB) in barley and wheat is reviewed. This disease, which can reach epidemic proportions under certain climatic conditions, is caused by various Fusarium species and affects grain yield and quality detrimentally, resulting in important economic losses in both crops. Furthermore, FHB infection poses a serious threat to human and animal health, due to the presence of toxic trichothecenes, of which deoxynivalenol and its derivatives appear to be the most important. Marker-based mapping studies have identifi ed numerous quantitative trait loci (QTLs) for FHB resistance, located on all the chromosomes of both species. Only a relatively small number of these can be detected consistently over a wide range of different environments and genetic backgrounds. None the less, where genetic effects have been characterized, they have been shown to be mainly additive in nature, meaning that the accumulation of several QTL factors in a single line ought to be effective in achieving raised levels of resistance. Indeed, marker-assisted selection has been directly shown to be feasible for some QTL. A number of QTLs for FHB resistance are associated with other agronomic characters, such as heading date (HD), fl owering time and plant height. In some cases, QTL alleles favourable for resistance are associated detrimentally with alleles for these characters, although there appear to be suffi ciently large numbers of QTLs for resistance acting independently of these characters to imply that reasonable genetic gains for resistance ought to be achievable in the future. While most studies in barley have addressed Type I resistance (initial infection) and in wheat Type II (spread between spikelets), or a combination of both Type I and Type II, more recent studies have addressed other types of resistance, such as Type III (effects on kernel size and characteristics), Type IV (yield tolerance) and Type V (decomposition or non-accumulation of mycotoxins such as deoxynivalenol). Besides identifying additional QTLs, these latter studies offer insights into the mechanisms of the different types of resistance observed, in some cases blurring the distinctions between them. Other prospects for improvement in FHB resistance, additional to those offered by marker-assisted selection, are also discussed.