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SummaryFusarium graminearum  produces the mycotoxin deoxynivalenol (DON) which promotes its expansion during infection on its plant host wheat. Conditional expression of DON production during infection is poorly characterized.  Wheat produces the defense compound putrescine, which induces hypertranscription of DON biosynthetic genes ( FgTRI s) and subsequently leads to DON accumulation during infection. Further, the regulatory mechanisms of  FgTRI s hypertranscription upon putrescine treatment were investigated.  The transcription factor FgAreA regulates putrescine‐mediated transcription of  FgTRI s by facilitating the enrichment of histone H2B monoubiquitination (H2B ub1) and histone 3 lysine 4 di‐ and trimethylations (H3K4 me2/3) on  FgTRIs . Importantly, a DNA‐binding domain (bZIP) specifically within the  Fusarium  H2B ub1 E3 ligase Bre1 othologs is identified, and the binding of this bZIP domain to  FgTRIs  depends on FgAreA‐mediated chromatin rearrangement. Interestingly, H2B ub1 regulates H3K4 me2/3 via the methyltransferase complex COMPASS component FgBre2, which is different from  Saccharomyces cerevisiae .  Taken together, our findings reveal the molecular mechanisms by which host‐generated putrescine induces DON production during  F. graminearum  infection. Our results also provide a novel insight into the role of putrescine during phytopathogen–host interactions and broaden our knowledge of H2B ub1 biogenesis and crosstalk between H2B ub1 and H3K4 me2/3 in eukaryotes.

Plant defense compound triggers mycotoxin synthesis by regulating H2B ub1 and H3K4 me2/3 deposition