ArticlePlant molecular biology2017
Metabolo-transcriptome profiling of barley reveals induction of chitin elicitor receptor kinase gene (HvCERK1) conferring resistance against Fusarium graminearum.
Article in Plant molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 64 citations in OpenAlex.
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- The maize ZmMIEL1 E3 ligase and ZmMYB83 transcription factor proteins interact and regulate the hypersensitive defence response.Molecular plant pathology · 2021Article
- Bioactive Components in Oat and Barley Grain as a Promising Breeding Trend for Functional Food Production.Molecules (Basel, Switzerland) · 2021Review
- Overexpression of a Cytochrome P450 Monooxygenase Involved in Orobanchol Biosynthesis Increases Susceptibility to Fusarium Head Blight.Frontiers in plant science · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
key messageWe report plausible disease resistance mechanisms induced by barley resistant genotype CI89831 against Fusarium head blight (FHB) based on metabolo-transcriptomics approach. We identified HvCERK1 as a candidate gene for FHB resistance, which is functional in resistant genotype CI9831 but non-functional in susceptible cultivars H106-371 and Zhedar-2. For the first time, we were able to show a hierarchy of regulatory genes that regulated downstream biosynthetic genes that eventually produced resistance related metabolites that reinforce the cell walls to contain the pathogen progress in plant. The HvCERK1 can be used for replacing in susceptible commercial cultivars, if non-functional, based on genome editing. Fusarium head blight (FHB) management is a great challenge in barley and wheat production worldwide. Though barley genome sequence and advanced omics technologies are available, till date none of the resistance mechanisms has been clearly deciphered. Hence, this study was aimed at identifying candidate gene(s) and elucidating resistance mechanisms induced by barley resistant genotype CI9831 based on integrated metabolomics and transcriptomics approach. Following Fusarium graminearum infection, we identified accumulation of specific set of induced secondary metabolites, belonging to phenylpropanoid, hydroxycinnamic acid (HCAA) and jasmonic acid pathways, and their biosynthetic genes. In association with these, receptor kinases such as chitin elicitor receptor kinase (HvCERK1) and protein kinases such as MAP kinase 3 (HvMPK3) and MAPK substrate 1 (HvMKS1), and transcription factors such as HvERF1/5, HvNAC42, HvWRKY23 and HvWRKY70 were also found upregulated with high fold change. Polymorphism studies across three barley genotypes confirmed the presence of mutations in HvCERK1 gene in two susceptible genotypes, isolating this gene as a potential candidate for FHB resistance. Further, the silencing of functional HvCERK1 gene in the resistant genotype CI9831, followed by gene expression and metabolite analysis revealed its role as an elicitor recognition receptor that triggered downstream regulatory genes, which in turn, regulated downstream metabolic pathway genes to biosynthesize resistance related (RR) metabolites to contain the pathogen to spikelet infection. A putative model on metabolic pathway regulation is proposed.
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