ENAP1 retrains seed germination via H3K9 acetylation mediated positive feedback regulation of ABI5.

ENAP1 retrains seed germination via H3K9 acetylation mediated positive feedback regulation of ABI5.
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DOI:
10.1371/journal.pgen.1009955
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发表时间:
2021-12
期刊:
影响因子:
4.5
通讯作者:
Qiao H
Qiao H
中科院分区:
生物学2区
文献类型:
--
作者:
Zhao B;Wang L;Shao Z;Chin K;Chakravarty D;Qiao H

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组蛋白乙酰化参与种子萌发的调控。转录因子ABI5在ABA抑制种子萌发过程中起着重要作用。然而,ABI5和组蛋白乙酰化如何在种子萌发过程中协同调控基因表达的分子机制仍然不清楚。在这里,我们证明了ENAP1与ABI5相互作用,并与包括ABI5本身在内的ABA反应基因共同结合。通过abi5零突变恢复了ENAP1ox种子萌发对ABA的敏感性。ABA促进H3K9Ac在启动子区域的浓缩以及与ENAP1和ABI5共同结合的靶基因的转录,这需要ENAP1和ABI5。ABI5基因受ENAP1和ABI5的直接调控。在enap1缺失的突变体中,H3K9Ac的丰度和ABI5在其自身启动子区域的结合活性以及ABI5的转录和蛋白水平都降低了;而在abi5-1突变体中,ABI5启动子的H3K9Ac丰度和ENAP1结合活性都降低了,这表明ENAP1和ABI5共同调节ABI5介导的正反馈调节。总之,我们的研究揭示了ENAP1调节H3K9乙酰化和介导ABI5正反馈调节抑制种子萌发的新的分子机制。为了优化开花植物在自然环境中的适应性,开花植物在良好的环境中引发种子萌发,并在胁迫条件下保持种子休眠。已经进化出精确的机制来调节发芽时间,以确保植物对不利环境的适应。脱落酸(ABA)是植物体内的一种主要应激激素,可诱导种子休眠,抑制种子萌发。已知表观遗传调控参与了ABA信号转导,其中转录因子ABI5起调控枢纽的作用。然而,组蛋白乙酰化等对ABI5转录的表观遗传调控仍然难以捉摸。在这项研究中,我们揭示了组蛋白结合蛋白ENAP1调节H3K9乙酰化的新的分子机制,该机制以ABI5依赖的方式介导ABI5的正反馈调节以抑制种子萌发。
Histone acetylation is involved in the regulation of seed germination. The transcription factor ABI5 plays an essential role in ABA- inhibited seed germination. However, the molecular mechanism of how ABI5 and histone acetylation coordinate to regulate gene expression during seed germination is still ambiguous. Here, we show that ENAP1 interacts with ABI5 and they co-bind to ABA responsive genes including ABI5 itself. The hypersensitivity to ABA of ENAP1ox seeds germination is recovered by the abi5 null mutation. ABA enhances H3K9Ac enrichment in the promoter regions as well as the transcription of target genes co-bound by ENAP1 and ABI5, which requires both ENAP1 and ABI5. ABI5 gene is directly regulated by ENAP1 and ABI5. In the enap1 deficient mutant, H3K9Ac enrichment and the binding activity of ABI5 in its own promoter region, along with ABI5 transcription and protein levels are all reduced; while in the abi5-1 mutant, the H3K9Ac enrichment and ENAP1 binding activity in ABI5 promoter are decreased, suggesting that ENAP1 and ABI5 function together to regulate ABI5- mediated positive feedback regulation. Overall, our research reveals a new molecular mechanism by which ENAP1 regulates H3K9 acetylation and mediates the positive feedback regulation of ABI5 to inhibit seed germination. To optimize the fitness in natural environment, flowering plants initiate seed germination in the favorable environment and maintain seed dormancy under stressful conditions. Precise mechanisms have been evolved to regulate germination timing to ensure plant adaptation to unfavorable environment. ABA, a major stress hormone in plants, induces seed dormancy and represses seed germination. Epigenetic regulation has been known involved in ABA signaling in which the transcription factor ABI5 acts as a regulatory hub. However, the epigenetic regulation such as histone acetylation on ABI5 transcription remains elusive. In this study, we revealed a new molecular mechanism by which histone binding protein ENAP1 regulates H3K9 acetylation, which mediates the positive feedback regulation of ABI5 in an ABI5 dependent manner to inhibit seed germination.
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