Wheat produces the defense compound putrescine, which induces hypertranscription of DON biosynthetic genes ( The transcription factor FgAreA regulates putrescine‐mediated transcription of Taken together, our findings reveal the molecular mechanisms by which host‐generated putrescine induces DON production during
Plant pathogens are challenged by host-derived iron starvation or excess during infection, but the mechanism through which pathogens counteract iron stress is unclear. Here, we found that Fusarium graminearum encounters iron excess during the colonization of wheat heads. Deletion of heme activator protein X (FgHapX), siderophore transcription factor A (FgSreA) or both attenuated virulence. Further, we found that FgHapX activates iron storage under iron excess by promoting histone H2B deubiquitination (H2B deub1) at the promoter of the responsible gene. Meanwhile, FgSreA is shown to inhibit genes mediating iron acquisition during iron excess by facilitating the deposition of histone variant H2A.Z and histone 3 lysine 27 trimethylation (H3K27 me3) at the first nucleosome after the transcription start site. In addition, the monothiol glutaredoxin FgGrx4 is responsible for iron sensing and control of the transcriptional activity of FgHapX and FgSreA via modulation of their enrichment at target genes and recruitment of epigenetic regulators, respectively. Taken together, our findings elucidated the molecular mechanisms for adaptation to iron excess mediated by FgHapX and FgSreA during infection in F. graminearum and provide novel insights into regulation of iron homeostasis at the chromatin level in eukaryotes.
more » « less- PAR ID:
- 10451637
- Publisher / Repository:
- Oxford University Press
- Date Published:
- Journal Name:
- Nucleic Acids Research
- Volume:
- 51
- Issue:
- 19
- ISSN:
- 0305-1048
- Format(s):
- Medium: X Size: p. 10238-10260
- Size(s):
- p. 10238-10260
- Sponsoring Org:
- National Science Foundation
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Summary Fusarium 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.FgTRI s) and subsequently leads to DON accumulation during infection. Further, the regulatory mechanisms ofFgTRI s hypertranscription upon putrescine treatment were investigated.FgTRI s by facilitating the enrichment of histone H2B monoubiquitination (H2B ub1) and histone 3 lysine 4 di‐ and trimethylations (H3K4 me2/3) onFgTRIs . Importantly, a DNA‐binding domain (bZIP) specifically within theFusarium H2B ub1 E3 ligase Bre1 othologs is identified, and the binding of this bZIP domain toFgTRIs depends on FgAreA‐mediated chromatin rearrangement. Interestingly, H2B ub1 regulates H3K4 me2/3 via the methyltransferase complex COMPASS component FgBre2, which is different fromSaccharomyces cerevisiae .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. -
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