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Brueggeman, R. S.

Publications and source records attributed to Brueggeman, R. S..

8 recordsLinked to original sources

A subset of world barley collection was used in the identification of sources of resistance and marker-trait association for resistance for bacterial leaf streak

The bacterial leaf streak (BLS) disease of barley, caused by Xanthomonas translucens pv. translucens (Xtt), has become increasingly important worldwide in recent years. Inefficacy of chemical control methods leaves deployment of host resistance to be the only option to manage this disease. However, current commercial varieties are mainly susceptible to BLS. Therefore, our goal was to identify sources of resistance from diverse barley germplasms and map associated genetic factors. To do so, we evaluated a subset of the World Barley Core Collection (BCC), consisting of 198 accessions, on their reaction to BLS from 2013 to 2016 under natural or artificially inoculated disease pressures. Ten accessions exhibited consistently low disease severities over four years of evaluations. Using genotype data from the T3/Barley database, genome-wide association studies were conducted to identify marker-trait associations (MTAs) in this barley mini-core panel for BLS resistance. Utilizing four mixed-model analyses (MLM, MLMM, FarmCPU, BLINK), five significant MTAs were consistently identified from at least two mixed model analyses including two in chromosome 2H, and one each in chromosomes 5H, and 7H. Associations in chromosomes 2H and 5H appear to be in the same region with loci identified in a previous association study, reinforcing their potential relevance. The identified resistant barley accessions and associated markers will be valuable inbreeding BLS-resistant barley varieties. Core ideas- A subset of world barley collection was used in the identification of sources of resistance and marker-trait association for resistance for bacterial leaf streak. - Ten accessions consistently showed low disease severity across different years, highlighting their value in BLS resistance breeding. - Five MTAs were consistently identified using different models, with two aligning with previously identified resistance QTLs.

plant biology↗

Rpt5 encodes a receptor-like protein that provides broad and effective net form net blotch (Pyrenophora teres f. teres) resistance in barley

The foliar disease net form net blotch (NFNB), caused by the necrotrophic fungal pathogen Pyrenophora teres f. teres (Ptt), causes significant yield and quality losses of barley worldwide. Dominant resistance conferred by the Resistance to Pyrenophora teres 5(Rpt5) gene from barley line CI5791 is the broadest and most effective resistance reported in this pathosystem. The Rpt5 locus was identified in multiple independent genetic studies utilizing diverse host populations and Ptt isolates, and harbors both dominant Rpt5 resistance and isolate-specific susceptibility genes/alleles that are dominant in the absence of Rpt5, designated susceptibility to Pyrenophora teres 1 (Spt1). Ptt virulence and avirulence effectors from diverse pathogen isolates genetically interact with the Rpt5/Spt1 locus, suggesting a complex locus with a function targeted by the evolution of a diversity of pathogen effectors. High-resolution mapping utilizing 1,920 recombinant gametes from a CI5791 x Tifang biparental population, identified 12 candidate genes in an [~]4.6 Mb delimited region in the cv Morex V3 genome assembly, but is 1.1 - 2.2 Mb in the pangenome assemblies, containing 5-12 genes. Analysis revealed a strong correlation between the CI5791 allele of a receptor-like protein (RLP), provisionally designated Rpt5 candidate gene 1, (Rcg1), and broad Rpt5-mediated resistance. Two independent transformants of the CI5791 Rcg1 allele in the susceptible cv Golden Promise background showed significantly increased resistance when challenged with Rpt5 avirulent Ptt isolates 6A, 15A, and 0-1 compared to the Golden Promise wildtype. Thus, Rpt5, encodes an RLP and is the first net blotch resistance gene cloned in barley. Significance StatementNet form net blotch (NFNB) causes substantial yield and quality losses of barley worldwide. Despite decades of ongoing research into genetic resistance to Pyrenophora teres f. teres, the causal agent of NFNB, no host resistance or susceptibility genes in this pathosystem had been previously identified. We present the identification and validation of Rpt5, which confers the broadest and most effective resistance against NFNB. To our knowledge Rpt5 is the first genetically defined resistance gene in a monocot to encode an RLP.

plant biology↗

High resolution mapping of novel non-transgressive hybrid susceptibility in barley exploited by P. teres f. maculata maps to a single pentatricopeptide repeat-containing protein

Hybrid genotypes can provide significant yield gains over conventional inbred varieties due to heterosis or hybrid vigor. However, hybrids can also display unintended negative attributes or phenotypes such as extreme pathogen susceptibility. The necrotrophic pathogen Pyrenophora teres f. maculata (Ptm) causes spot form net blotch, which has caused significant losses to barley worldwide. Here, we report on a non-transgressive hybrid susceptibility locus in barley initially recognized because the three parental lines CI5791, Tifang and Golden Promise are resistant to Ptm isolate 13IM.3, however F2 progeny from CI5791 x Tifang and CI5791 x Golden Promise crosses exhibited extreme susceptibility. The susceptible phenotype segregated in a ratio of 1 resistant:1 susceptible representing a genetic segregation ratio of 1 parental (res):2 heterozygous (sus):1 parental (res) suggesting a single hybrid susceptibility locus. Genetic mapping using a total of 715 CI5791 x Tifang F2 individuals (1430 recombinant gametes) and 149 targeted SNPs delimited the hybrid susceptibility locus designated Susceptibility to Pyrenophora teres 2 (Spt2) to an [~]198 kb region on chromosome 5H of the Morex V3 reference assembly. This single locus was independently mapped with 83 CI5791 x Golden Promise F2 individuals (166 recombinant gametes) and 180 genome wide SNPs that colocalized to the same Spt2 locus. The CI5791 genome was sequenced using PacBio Continuous Long Read technology and comparative analysis between CI5791 and the publicly available Golden Promise genome assembly determined that the delimited region contained a single high confidence Spt2 candidate gene predicted to encode a pentatricopeptide repeat-containing protein.

plant biology↗

Pathogen genetics identifies avirulence/virulence loci associated with barley chromosome 6H resistance in the Pyrenophora teres f. teres - barley interaction

Barley net form net blotch (NFNB) is a foliar disease caused by Pyrenophora teres f. teres. Barley line CIho5791, which harbors the chromosome 6H broad spectrum resistance gene Rpt5, displays dominant resistance to P. teres f. teres. To genetically characterize P. teres f. teres avirulence/virulence on the barley line CIho5791, we generated a P. teres f. teres mapping population using a cross between the Moroccan CIho5791-virulent isolate MorSM40-3, and the avirulent reference isolate 0-1. Genetic maps were generated for all 12 chromosomes (Ch) and quantitative trait locus (QTL) mapping identified two significant QTL associated with P. teres f. teres avirulence/virulence on CIho5791. The most significant QTL mapped to P. teres f. teres Ch1 where the virulent allele was contributed by MorSM40-3. A second QTL mapped to Ch8, however, this virulent allele was contributed by 0-1. The Ch1 and Ch8 loci accounted for 27 and 15% of the disease variation, respectively and the avirulent allele at the Ch1 locus was shown to be epistatic over the virulent allele at the Ch8 locus. Additionally, we used 177 sequenced P. teres f. teres isolates in a genome wide association study that identified the same Ch1 and Ch8 loci as the two most significant associations. Within the identified genomic regions, we identified several genes that encoded small secreted proteins, one or more of which may be responsible for overcoming the CIho5791 resistance. Results presented here demonstrate the complexity of avirulence/virulence in the P. teres f. teres - barley interaction.

genetics↗

Genome wide association mapping of Pyrenophora teres f. maculata and Pyrenophora teres f. teres resistance loci utilizing natural Turkish wild and landrace barley populations

Unimproved landraces and wild relatives of crops are sources of genetic diversity that were lost post domestication in modern breeding programs. To tap into this rich resource, genome wide association studies in large plant genomes have enabled the rapid genetic characterization of desired traits from natural landrace and wild populations. Wild barley (Hordeum spontaneum), the progenitor of domesticated barley (H. vulgare), is dispersed across Asia and North Africa, and has co-evolved with the ascomycetous fungal pathogens Pyrenophora teres f. teres and P. teres f. maculata, the casual agents of the diseases net form of net blotch and spot form of net blotch, respectively. Thus, these wild and local adapted barley landraces from the region of origin of both the host and pathogen represent a diverse gene pool to identify new sources of resistance, due to millions of years of co-evolution. The barley - P. teres pathosystem is governed by complex genetic interactions with dominant, recessive, and incomplete resistances and susceptibilities, with many isolate-specific interactions. Here we provide the first genome wide association study of wild and landrace barley from the Fertile Crescent for resistance to both forms of P. teres. A total of 14 loci, four against P. teres f. maculata and ten against Pyrenophora teres f. teres, were identified in both wild and landrace populations, showing that both are genetic reservoirs for novel sources of resistance. We also highlight the importance of using multiple algorithms to both identify and validate additional loci.

genetics↗

Localization of hyphal growth associated with mycotoxin production during the malting of Fusarium head blight infected grains

Fusarium head blight (FHB) and the occurrence of mycotoxins is the largest food safety threat to malting and brewing grains. Objectives of the current study were to localize the growth of Fusarium within FHB infected kernels and to associate it with the production of DON that occurred during malting. FHB infected barley, wheat, rye, and triticale grains that exhibited large increases in Fusarium Tri5 DNA and trichothecene mycotoxins following malting, were screened for hyphal localization. The growth of hyphae, both on the surface of kernels and within tissues of grain and malt was, imagined by scanning electron microscopy and confocal laser scanning microscopy assisted with WGA-Alexa Fluor 488 pre-staining, respectively. In barley, hyphae were primarily present on or within husk, vascular bundle, and pericarp cavities. Following malting, large amounts of hyphal growth were observed in not only these regions, but also in the aleurone layer, endosperm, and embryo. Extensive fungal growth was also observed following malting of wheat, rye, and triticale. Interestingly, these grains already had an extensive internal presence of hyphae in unmalted grain, occurring in the pericarp, testa, vascular bundle, nucellar projection, aleurone layer, endosperm, pericarp and endosperm cavities, and embryo. Shotgun sequencing followed by metagenomics analysis verified that Fusarium spp. accounted for above 90% of the fungal hyphae growing in the interior of grains during malting, which coincided with the significant production of mycotoxins.

plant biology↗

rcs5-mediated spot blotch resistance in barley is conferred by wall-associated kinases that resist pathogen manipulation

Plant biotrophic pathogen disease resistances rely on immunity receptor-mediated programmed cell death (PCD) responses, but specialized necrotrophic/hemi-biotrophic pathogens hijack these mechanisms to colonize the resulting dead tissue in their necrotrophic phase. Thus, immunity receptors can become necrotrophic pathogen dominant susceptibility targets but resistance mechanisms that resist necrotroph manipulation are recessive resistance genes. The barley rcs5 QTL imparts recessive resistance against the disease spot blotch caused by the hemi-biotrophic fungal pathogen Bipolaris sorokiniana. The rcs5 genetic interval was delimited to ~0.23 cM, representing an ~234 kb genomic region containing four wall-associated kinase (WAK) genes, designated HvWak2, Sbs1, Sbs2 (susceptibility to Bipolaris sorokiniana 1&2), and HvWak5. Post-transcriptional gene silencing of Sbs1&2 in susceptible barley cultivars resulted in resistance showing dominant susceptibility function. Allele analysis of Sbs1&2 from resistant and susceptible barley cultivars identified sequence polymorphisms associated with phenotypes in their primary coding sequence and promoter regions, suggesting differential transcriptional regulation may contribute to susceptibility. Transcript analysis of Sbs1&2 showed nearly undetectable expression in resistant and susceptible cultivars prior to pathogen challenge; however, upregulation of both genes occurred specifically in susceptible cultivars post-inoculation with a virulent isolate. Apoplastic wash fluids collected from barley infected with a virulent isolate induced Sbs1, suggesting regulation by an apoplastic-secreted effector. Thus, Sbs1&2 function as B. sorokiniana susceptibility targets and non-functional alleles or alleles that resist induction by the pathogen mediate rcs5-recessive resistance. The sbs1&2 alleles underlying the rcs5 QTL that the pathogen is unable to manipulate are the first resistance genes identified against spot blotch. SIGNIFICANCE STATEMENTThe rcs5 locus in barley confers a high level of seedling resistance and a moderate level of adult plant resistance to spot blotch. It is part of a complex that has provided durable spot blotch resistance in many North American barley cultivars (cv) for more than 50 years. Genetic characterization and positional cloning of rcs5 identified the dominant susceptibility genes, Sbs1 and Sbs2 (susceptibility to Bipolaris sorokiniana 1 and 2) as wall-associated kinases. These genes are hijacked by the hemibiotrophic pathogen in its necrotrophic phase to induce programmed cell death, facilitating disease development. We report the first spot blotch resistance/susceptibility genes cloned that function via alleles that cannot be specifically induced and hijacked by virulent isolates of the pathogen.

plant biology↗

A comparative genomic analysis of the barley pathogen Pyrenophora teres f. teres identifies sub-telomeric regions as drivers of virulence

Pyrenophora teres f. teres causes net form net blotch of barley and is an economically important pathogen throughout the world. However, P. teres f. teres is lacking in the genomic resources necessary to characterize the mechanisms of virulence. Recently a high quality reference genome was generated for P. teres f. teres isolate 0-1. Here, we present the reference quality sequence and annotation of four new isolates and we use the five available P. teres f. teres genomes for an in-depth comparison resulting in the generation of hypotheses pertaining to the potential mechanisms and evolution of virulence. Comparative analyses were performed between all five P. teres f. teres genomes examining genomic organization, structural variations, and core and accessory genomic content, specifically focusing on the genomic characterization of known virulence loci and the localization of genes predicted to encode secreted and effector proteins. We showed that 14 of 15 currently published virulence quantitative trait loci (QTL) span accessory genomic regions consistent with these accessory regions being important drivers of host adaptation. Additionally, these accessory genomic regions were frequently found in sub-telomeric regions of chromosomes with 10 of the 14 accessory region QTL localizing to sub-telomeric regions. Comparative analysis of the sub-telomeric regions of P. teres f. teres chromosomes revealed translocation events where homology was detected between non-homologous chromosomes at a significantly higher rate than the rest of the genome. These results indicate that the sub-telomeric accessory genomic compartments not only harbor most of the known virulence loci, but also that these regions have the capacity to rapidly evolve.

genomics↗