<p>Fusarium Head Blight (FHB) is a devastating fungal disease of small grain cereals like wheat and barley, causing substantial yield and quality losses each year worldwide. FHB is caused by <i>Fusarium</i> species that produce mycotoxins such as deoxynivalenol (DON) that impairs protein biosynthesis. Although defense responses in barley to Fusarium infection have been described at the transcriptional level, it remains unclear to what extent these responses are translated into functional changes at the protein and metabolite levels.</p><p>In this study, we employed comprehensive transcriptomics, proteomics, and metabolomics to dissect the defense responses of barley heads during infection with <i>Fusarium culmorum</i>. Our integrated analyses revealed a set of significantly regulated gene-protein pairs linked to biosynthetic pathways that consistently correspond to upregulated defense-related metabolites. These include tryptophan-derived stress metabolites such as tryptamine and serotonin, as well as barley-specific hydroxycinnamylamides, including conjugates from the trypthophan metabolism, hordatines, and their biosynthetic precursors.</p><p>Integrating data across multiple omics layers identifies the upregulation of aromatic amino acid derived secondary metabolism as the most consistent barley response to FHB infection across diverse barley varieties that share barley-typical type II resistance to fungal spreading in the head rachis.</p>

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Multi-omics of barley Fusarium Head Blight converge on pathogen-triggered biosynthesis of aromatic amino acid derived chemical defense compounds

  • Sophia Hein,
  • Christina E. Steidele,
  • Felix Hoheneder,
  • Sarah Brajkovic,
  • Bernhard Kuster,
  • Lisa Kurzweil,
  • Timo D. Stark,
  • Corinna Dawid,
  • Ralph Hückelhoven

摘要

Fusarium Head Blight (FHB) is a devastating fungal disease of small grain cereals like wheat and barley, causing substantial yield and quality losses each year worldwide. FHB is caused by Fusarium species that produce mycotoxins such as deoxynivalenol (DON) that impairs protein biosynthesis. Although defense responses in barley to Fusarium infection have been described at the transcriptional level, it remains unclear to what extent these responses are translated into functional changes at the protein and metabolite levels.

In this study, we employed comprehensive transcriptomics, proteomics, and metabolomics to dissect the defense responses of barley heads during infection with Fusarium culmorum. Our integrated analyses revealed a set of significantly regulated gene-protein pairs linked to biosynthetic pathways that consistently correspond to upregulated defense-related metabolites. These include tryptophan-derived stress metabolites such as tryptamine and serotonin, as well as barley-specific hydroxycinnamylamides, including conjugates from the trypthophan metabolism, hordatines, and their biosynthetic precursors.

Integrating data across multiple omics layers identifies the upregulation of aromatic amino acid derived secondary metabolism as the most consistent barley response to FHB infection across diverse barley varieties that share barley-typical type II resistance to fungal spreading in the head rachis.