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

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Mapping quantitative trait loci associated with leaf rust resistance in five spring wheat populations using single nucleotide polymorphism markers

Growing resistant wheat (Triticum aestivum L) varieties is an important strategy for the control of leaf rust, caused by Puccinia triticina Eriks. This study sought to identify the chromosomal location and effects of leaf rust resistance loci in five Canadian spring wheat cultivars. The parents and doubled haploid lines of crosses Carberry/AC Cadillac, Carberry/Vesper, Vesper/Lillian, Vesper/Stettler and Stettler/Red Fife were assessed for leaf rust severity and infection response in field nurseries in Canada near Swift Current, SK from 2013 to 2015, Morden, MB from 2015 to 2017 and Brandon, MB in 2016, and in New Zealand near Lincoln in 2014. The populations were genotyped with the 90K Infinium iSelect assay and quantitative trait loci (QTL) analysis was performed. A high density consensus map generated based on 14 doubled haploid populations and integrating SNP and SSR markers was used to compare QTL identified in different populations. AC Cadillac contributed QTL on chromosomes 2A, 3B and 7B (2 loci), Carberry on 1A, 2B (2 loci), 2D, 4B (2 loci), 5A, 6A, 7A and 7D, Lillian on 4A and 7D, Stettler on 2D and 6B, Vesper on 1B, 1D, 2A, 6B and 7B (2 loci), and Red Fife on 7A and 7B. Lillian contributed to a novel locus QLr.spa-4A, and similarly Carberry at QLr.spa-5A. The discovery of novel leaf rust resistance QTL QLr.spa-4A and QLr.spa-5A, and several others in contemporary Canada Western Red Spring wheat varieties is a tremendous addition to our present knowledge of resistance gene deployment in breeding. Carberry demonstrated substantial stacking of genes which could be supplemented with the genes identified in other cultivars with the expectation of increasing efficacy of resistance to leaf rust and longevity with little risk of linkage drag

Genetic and transcriptional dissection of resistance to Claviceps purpurea in the durum wheat cultivar Greenshank.

Funder: Canadian Seed Growers' Association; doi: http://dx.doi.org/10.13039/501100000071Funder: National Research Council of Canada: Canadian Wheat Improvement programFour QTL for ergot resistance (causal pathogen Claviceps purpurea) have been identified in the durum wheat cultivar Greenshank. Claviceps purpurea is a pathogen of grasses that infects flowers, replacing the seed with an ergot sclerotium. Ergot presents a significant problem to rye, barley and wheat, in particular hybrid seed production systems. In addition, there is evidence that the highly toxic alkaloids that accumulate within sclerotia can cross-contaminate otherwise healthy grain. Host resistance to C. purpurea is rare, few resistance loci having been identified. In this study, four ergot resistance loci are located on chromosomes 1B, 2A, 5A and 5B in the durum wheat cv. Greenshank. Ergot resistance was assessed through analysis of phenotypes associated with C. purpurea infection, namely the number of inoculated flowers that produced sclerotia, or resulted in ovary death but no sclerotia, the levels of honeydew produced, total sclerotia weight and average sclerotia weight and size per spike. Ergot testing was undertaken in Canada and the UK. A major effect QTL, QCp.aafc.DH-2A, was detected in both the Canadian and UK experiments and had a significant effect on honeydew production levels. QCp.aafc.DH-5B had the biggest influence on total sclerotia weight per spike. QCp.aafc.DH-1B was only detected in the Canadian experiments and QCp.aafc.DH-5A in the UK experiment. An RNASeq analysis, undertaken to identify wheat differentially expressed genes associated with different combinations of the four ergot resistance QTL, revealed a disproportionate number of DEGs locating to the QCp.aafc.DH-1B, QCp.aafc.DH-2A and QCp.aafc.DH-5B QTL intervals

A Consensus Map in Cultivated Hexaploid Oat Reveals Conserved Grass Synteny with Substantial Subgenome Rearrangement

Hexaploid oat ( L., 2 = 6 = 42) is a member of the Poaceae family and has a large genome (∼12.5 Gb) containing 21 chromosome pairs from three ancestral genomes. Physical rearrangements among parental genomes have hindered the development of linkage maps in this species. The objective of this work was to develop a single high-density consensus linkage map that is representative of the majority of commonly grown oat varieties. Data from a cDNA-derived single-nucleotide polymorphism (SNP) array and genotyping-by-sequencing (GBS) were collected from the progeny of 12 biparental recombinant inbred line populations derived from 19 parents representing oat germplasm cultivated primarily in North America. Linkage groups from all mapping populations were compared to identify 21 clusters of conserved collinearity. Linkage groups within each cluster were then merged into 21 consensus chromosomes, generating a framework consensus map of 7202 markers spanning 2843 cM. An additional 9678 markers were placed on this map with a lower degree of certainty. Assignment to physical chromosomes with high confidence was made for nine chromosomes. Comparison of homeologous regions among oat chromosomes and matches to orthologous regions of rice ( L.) reveal that the hexaploid oat genome has been highly rearranged relative to its ancestral diploid genomes as a result of frequent translocations among chromosomes. Heterogeneous chromosome rearrangements among populations were also evident, probably accounting for the failure of some linkage groups to match the consensus. This work contributes to a further understanding of the organization and evolution of hexaploid grass genomes

Integrated Metabolo-Transcriptomics Reveals Fusarium Head Blight Candidate Resistance Genes in Wheat QTL-Fhb2

<div><p>Background</p><p>Fusarium head blight (FHB) caused by <i>Fusarium graminearum</i> not only causes severe losses in yield, but also reduces quality of wheat grain by accumulating mycotoxins. Breeding for host plant resistance is considered as the best strategy to manage FHB. Resistance in wheat to FHB is quantitative in nature, involving cumulative effects of many genes governing resistance. The poor understanding of genetics and lack of precise phenotyping has hindered the development of FHB resistant cultivars. Though more than 100 QTLs imparting FHB resistance have been reported, none discovered the specific genes localized within the QTL region, nor the underlying mechanisms of resistance.</p><p>Findings</p><p>In our study recombinant inbred lines (RILs) carrying resistant (R-RIL) and susceptible (S-RIL) alleles of QTL-Fhb2 were subjected to metabolome and transcriptome profiling to discover the candidate genes. Metabolome profiling detected a higher abundance of metabolites belonging to phenylpropanoid, lignin, glycerophospholipid, flavonoid, fatty acid, and terpenoid biosynthetic pathways in R-RIL than in S-RIL. Transcriptome analysis revealed up-regulation of several receptor kinases, transcription factors, signaling, mycotoxin detoxification and resistance related genes. The dissection of QTL-Fhb2 using flanking marker sequences, integrating metabolomic and transcriptomic datasets, identified 4-Coumarate: CoA ligase (<i>4CL</i>), callose synthase (<i>CS</i>), basic Helix Loop Helix (<i>bHLH041</i>) transcription factor, glutathione S-transferase (<i>GST</i>), ABC transporter-4 (<i>ABC4</i>) and cinnamyl alcohol dehydrogenase (<i>CAD</i>) as putative resistance genes localized within the QTL-Fhb2 region.</p><p>Conclusion</p><p>Some of the identified genes within the QTL region are associated with structural resistance through cell wall reinforcement, reducing the spread of pathogen through rachis within a spike and few other genes that detoxify DON, the virulence factor, thus eventually reducing disease severity. In conclusion, we report that the wheat resistance QTL-Fhb2 is associated with high rachis resistance through additive resistance effects of genes, based on cell wall enforcement and detoxification of DON. Following further functional characterization and validation, these resistance genes can be used to replace the genes in susceptible commercial cultivars, if nonfunctional, based on genome editing to improve FHB resistance.</p></div

Mapping of Major Fusarium Head Blight Resistance from Canadian Wheat cv. AAC Tenacious

Fusarium head blight (FHB) is one of the most devastating wheat disease due to its direct detrimental effects on grain-yield, quality and marketability. Resistant cultivars offer the most effective approach to manage FHB; however, the lack of different resistance resources is still a major bottleneck for wheat breeding programs. To identify and dissect FHB resistance, a doubled haploid wheat population produced from the Canadian spring wheat cvs AAC Innova and AAC Tenacious was phenotyped for FHB response variables incidence and severity, visual rating index (VRI), deoxynivalenol (DON) content, and agronomic traits days to anthesis (DTA) and plant height (PHT), followed by single nucleotide polymorphism (SNP) and simple sequence repeat (SSR) marker genotyping. A high-density map was constructed consisting of 10,328 markers, mapped on all 21 chromosomes with a map density of 0.35 cM/marker. Together, two major quantitative trait loci for FHB resistance were identified on chromosome 2D from AAC Tenacious; one of these loci on 2DS also colocated with loci for DTA and PHT. Another major locus for PHT, which cosegregates with locus for low DON, was also identified along with many minor and epistatic loci. QTL identified from AAC Tenacious may be useful to pyramid FHB resistance

Transcriptome dynamics associated with resistance and susceptibility against fusarium head blight in four wheat genotypes

Abstract Background Fusarium head blight (FHB) of wheat in North America is caused mostly by the fungal pathogen Fusarium graminearum (Fg). Upon exposure to Fg, wheat initiates a series of cellular responses involving massive transcriptional reprogramming. In this study, we analyzed transcriptomics data of four wheat genotypes (Nyubai, Wuhan 1, HC374, and Shaw), at 2 and 4 days post inoculation (dpi) with Fg, using RNA-seq technology. Results A total of 37,772 differentially expressed genes (DEGs) were identified, 28,961 from wheat and 8811 from the pathogen. The susceptible genotype Shaw exhibited the highest number of host and pathogen DEGs, including 2270 DEGs associating with FHB susceptibility. Protein serine/threonine kinases and LRR-RK were associated with susceptibility at 2 dpi, while several ethylene-responsive, WRKY, Myb, bZIP and NAC-domain containing transcription factors were associated with susceptibility at 4 dpi. In the three resistant genotypes, 220 DEGs were associated with resistance. Glutathione S-transferase (GST), membrane proteins and distinct LRR-RKs were associated with FHB resistance across the three genotypes. Genes with unique, high up-regulation by Fg in Wuhan 1 were mostly transiently expressed at 2 dpi, while many defense-associated genes were up-regulated at both 2 and 4 dpi in Nyubai; the majority of unique genes up-regulated in HC374 were detected at 4 dpi only. In the pathogen, most genes showed increased expression between 2 and 4 dpi in all genotypes, with stronger levels in the susceptible host; however two pectate lyases and a hydrolase were expressed higher at 2 dpi, and acetyltransferase activity was highly enriched at 4 dpi. Conclusions There was an early up-regulation of LRR-RKs, different between susceptible and resistant genotypes; subsequently, distinct sets of genes associated with defense response were up-regulated. Differences in expression profiles among the resistant genotypes indicate genotype-specific defense mechanisms. This study also shows a greater resemblance in transcriptomics of HC374 to Nyubai, consistent with their sharing of two FHB resistance QTLs on 3BS and 5AS, compared to Wuhan 1 which carries one QTL on 2DL in common with HC374