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调控控制脱落酸分解代谢的进化保守表观遗传调控子可增强小麦的耐旱性。

Modulation of an evolutionarily conserved epigenetic regulon controlling abscisic acid catabolism enhances drought tolerance in wheat.

作者信息

Li Yunzhen, Jin Liujie, Li Wanying, Wang Ke, Su Handong, Mao Hailiang, Chen Wei, Lan Caixia, Li Qiang, Kaufmann Kerstin, Yan Wenhao

机构信息

National Key Laboratory of Crop Genetic Improvement, Hubei Hongshan Laboratory, Huazhong Agricultural University, Wuhan, 430070, China.

Plant Cell and Molecular Biology, Institute of Biology, Humboldt-Universität zu Berlin, Berlin, 10115, Germany.

出版信息

New Phytol. 2025 Aug;247(4):1777-1789. doi: 10.1111/nph.70302. Epub 2025 Jun 22.

Abstract

Drought stress significantly reduces crop yield by triggering abscisic acid (ABA) accumulation in plants. It involves the suppression of CYP707A genes, which encode enzymes that catalyze ABA. However, little is known about epigenetic control in the CYP707A gene-mediated drought stress response in wheat. In this study, we reported that TaCYP707A-6A/6B/6D but not TaCYP707A-5A/5B/5D participates in drought response in common wheat. Disruption of TaCYP707A-6B showed enhanced drought tolerance but also decreased fertility. Expression of TaCYP707A-6B is negatively associated with H3K27me3 level. An evolutionarily conserved CTCTGYTY motif cluster (binding site for a Jumonji H3K27me3 demethylase) was found in the intron of TaCYP707A-6B as well as the intron of CYP707A homologs in other plant species. Blocking the CTCTGYTY motif by dead Cas9 (dCas9) maintained a high level of H3K27me3 on the CYP707A gene, while decreasing its expression level leading to enhanced drought tolerance in both wheat and Arabidopsis. In particular, the mutant in which the intron bound by H3K27me3 demethylase was cut out without change of splicing pattern showed enhanced drought tolerance. Therefore, our study provides a novel approach to improve plant drought tolerance by manipulating an evolutionarily conserved cis-element bound by histone demethylases in the intron of CYP707A genes.

摘要

干旱胁迫通过触发植物体内脱落酸(ABA)积累显著降低作物产量。这涉及对CYP707A基因的抑制,该基因编码催化ABA的酶。然而,关于小麦中CYP707A基因介导的干旱胁迫响应中的表观遗传调控知之甚少。在本研究中,我们报道了TaCYP707A - 6A/6B/6D而非TaCYP707A - 5A/5B/5D参与普通小麦的干旱响应。TaCYP707A - 6B的破坏显示出增强的耐旱性,但也降低了育性。TaCYP707A - 6B的表达与H3K27me3水平呈负相关。在TaCYP707A - 6B的内含子以及其他植物物种中CYP707A同源物的内含子中发现了一个进化保守的CTCTGYTY基序簇(Jumonji H3K27me3去甲基化酶的结合位点)。用无活性的Cas9(dCas9)阻断CTCTGYTY基序可维持CYP707A基因上高水平的H3K27me3,同时降低其表达水平,从而导致小麦和拟南芥的耐旱性增强。特别是,通过切除由H3K27me3去甲基化酶结合的内含子而不改变剪接模式的突变体表现出增强的耐旱性。因此,我们的研究提供了一种通过操纵CYP707A基因内含子中由组蛋白去甲基化酶结合的进化保守顺式元件来提高植物耐旱性的新方法。

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