Genetic architecture of fusarium head blight disease resistance and associated traits in Nordic spring wheat.

KEY MESSAGE: This study identified a significant number of QTL that are associated with FHB disease resistance in NMBU spring wheat panel by conducting genome-wide association study. Fusarium head blight (FHB) is a widely known devastating disease of wheat caused by Fusarium graminearum and other Fusarium species. FHB resistance is quantitative, highly complex and divided into several resistance types. Quantitative trait loci (QTL) that are effective against several of the resistance types give valuable contributions to resistance breeding. A spring wheat panel of 300 cultivars and breeding lines of Nordic and exotic origins was tested in artificially inoculated field trials and subjected to visual FHB assessment in the years 2013-2015, 2019 and 2020. Deoxynivalenol (DON) content was measured on harvested grain samples, and anther extrusion (AE) was assessed in separate trials. Principal component analysis based on 35 and 25 K SNP arrays revealed the existence of two subgroups, dividing the panel into European and exotic lines. We employed a genome-wide association study to detect QTL associated with FHB traits and identify marker-trait associations that consistently influenced FHB resistance. A total of thirteen QTL were identified showing consistent effects across FHB resistance traits and environments. Haplotype analysis revealed a highly significant QTL on 7A, Qfhb.nmbu.7A.2, which was further validated on an independent set of breeding lines. Breeder-friendly KASP markers were developed for this QTL that can be used in marker-assisted selection. The lines in the wheat panel harbored from zero to five resistance alleles, and allele stacking showed that resistance can be significantly increased by combining several of these resistance alleles. This information enhances breeders´ possibilities for genomic prediction and to breed cultivars with improved FHB resistance.

The ASH1 HOMOLOG 2 (ASHH2) histone H3 methyltransferase is required for ovule and anther development in Arabidopsis.

BACKGROUND: SET-domain proteins are histone lysine (K) methyltransferases (HMTase) implicated in defining transcriptionally permissive or repressive chromatin. The Arabidopsis ASH1 HOMOLOG 2 (ASHH2) protein (also called SDG8, EFS and CCR1) has been suggested to methylate H3K4 and/or H3K36 and is similar to Drosophila ASH1, a positive maintainer of gene expression, and yeast Set2, a H3K36 HMTase. Mutation of the ASHH2 gene has pleiotropic developmental effects. Here we focus on the role of ASHH2 in plant reproduction. METHODOLOGY/PRINCIPAL FINDINGS: A slightly reduced transmission of the ashh2 allele in reciprocal crosses implied involvement in gametogenesis or gamete function. However, the main requirement of ASHH2 is sporophytic. On the female side, close to 80% of mature ovules lack embryo sac. On the male side, anthers frequently develop without pollen sacs or with specific defects in the tapetum layer, resulting in reduction in the number of functional pollen per anther by up to approximately 90%. In consistence with the phenotypic findings, an ASHH2 promoter-reporter gene was expressed at the site of megaspore mother cell formation as well as tapetum layers and pollen. ashh2 mutations also result in homeotic changes in floral organ identity. Transcriptional profiling identified more than 300 up-regulated and 600 down-regulated genes in ashh2 mutant inflorescences, whereof the latter included genes involved in determination of floral organ identity, embryo sac and anther/pollen development. This was confirmed by real-time PCR. In the chromatin of such genes (AP1, AtDMC1 and MYB99) we observed a reduction of H3K36 trimethylation (me3), but not H3K4me3 or H3K36me2. CONCLUSIONS/SIGNIFICANCE: The severe distortion of reproductive organ development in ashh2 mutants, argues that ASHH2 is required for the correct expression of genes essential to reproductive development. The reduction in the ashh2 mutant of H3K36me3 on down-regulated genes relevant to the observed defects, implicates ASHH2 in regulation of gene expression via H3K36 trimethylation in chromatin of Arabidopsis inflorescences.