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

Plant defense compound triggers mycotoxin synthesis by regulating H2B ub1 and H3K4 me2/3 deposition.
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植物防御化合物通过调节 H2B ub1 和 H3K4 me2/3 沉积触发霉菌毒素合成

DOI:
10.1111/nph.17718
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发表时间:
2021-12
期刊:
影响因子:
9.4
通讯作者:
Yin, Yanni
Yin, Yanni
中科院分区:
生物学1区
文献类型:
--
作者:
Ma, Tianling;Zhang, Lixin;Wang, Minhui;Li, Yiqing;Jian, Yunqing;Wu, Liang;Kistler, Harold Corby;Ma, Zhonghua;Yin, Yanni

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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. Wheat produces the defense compound putrescine, which induces hypertranscription of DON biosynthetic genes (FgTRIs) and subsequently leads to DON accumulation during infection. Further, the regulatory mechanisms of FgTRIs hypertranscription upon putrescine treatment were investigated. The transcription factor FgAreA regulates putrescine‐mediated transcription of FgTRIs 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.
DOI: 10.1080/03235400600914355
发表时间: 2009-01-01
影响因子: 1
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