阿拉伯芥組蛋白去甲基化酶 JMJ28 與組蛋白乙醯轉移酶 GCN5 相互作用並參與 ABA 反應

Abstract

組蛋白乙酰化、甲基化、泛素化和磷酸化修飾在基因表達的調控中起著重要作用，其中組蛋白乙酰化通常會促進基因表達。阿拉伯芥組蛋白乙酰轉移酶 GENERAL CONTROL NONDER EPRESSIBLE 5 (GCN5)，又稱為 HISTONE ACETYLTRANSFERASE OF THE GNAT FAMILY 1 (HAG1)，具有組蛋白 H3 賴氨酸 9 (H3K9) 和 H3 賴氨酸 14 (H3K14) 乙酰化活性，在植物發育和植物對生物脅迫的反應中起著至關重要的作用。組蛋白H3K9二甲基化 (H3K9me2) 是一種基因表達抑制性標記。JMJ28 是一種KDM3/JHDM2類群的包含jmjC結構域的組蛋白去甲基化酶，具有H3K9me2去甲基化活性。然而，尚不清楚植物在響應非生物脅迫時組蛋白H3K9去甲基化和組蛋白乙酰化之間是否存在交互作用。在本研究中，我們發現 JMJ28 和 GCN5 有交互作用並且參與脫落酸 (ABA) 反應。與 Col-0 野生型相比，在用 ABA 處理之後， ABA 反應基因 RD26、ABI2、RD29A 和 RD29B 的表達在jmj28，hac3-2 和 jmj28/hac3-2 突變體中降低。此外，JMJ28可直接結合在 RD26， ABI2 和 RD29A/B 基因上，並且JMJ28 的結合受 ABA 誘導。在 ABA 處理後，jmj28 和 jmj28/hac3-2 中 RD26，ABI2 和 RD29A/B 上的 H3K9me2 水平顯著高於 Col-0，表明 JMJ28 通過 H3K9me2 去甲基化激活基因表達。此外，jmj28，hac3-2 和 jmj28/hac3-2 中 RD26，ABI2 和 RD29A/B 上的 H3K9 乙酰化 (H3K9ac) 水平顯著降低，表明 JMJ28 正向調節 GCN5 介導的 H3K9ac。綜上所述，我們得出的結論是，ABA 可以通過JMJ 28去除抑制標記 H3K9me2 並添加由GCN5 所介導的活性標記 H3K9ac 來誘導基因表達。

Histone modifications including acetylation, methylation, ubiquitination and phosphorylation play important roles in the regulation of gene expression. Histone acetylation is usually associated with active gene expression. The Arabidopsis histone acetyltransferase GENERAL CONTROL NONDEREPRESSIBLE 5 (GCN5), also known as HISTONE ACETYLTRANSFERASE OF THE GNAT FAMILY 1 (HAG1), has histone H3 lysine 9 (H3K9) and H3K14 acetylation activity, which plays an essential role in plant development and plant response to abiotic stress. Histone H3 lysine 9 di-methylation (H3K9me2) is a transcriptional repressive mark. JMJ28, a KDM3/JHDM2 group JmjC domain-containing histone demethylase, has H3K9me2 demethylation activity. However, it is unclear whether there is a crosstalk between histone H3K9 demethylation and histone acetylation in plant response to abiotic stress. In this study, we found that JMJ28 and GCN5 interact and are involved in abscisic acid (ABA) response. Compared to Col-0 wild type, the expression of the ABA responsive genes RD26, ABI2, RD29A and RD29B is decreased in jmj28, hac3-2 and jmj28/hac3-2 mutants treated with ABA. Moreover, JMJ28 can directly bind to RD26, ABI2 and RD29A/B loci, and the binding of JMJ28 is induced by ABA. The levels of H3K9me2 on RD26, ABI2 and RD29A/B in jmj28 and jmj28/hac3-2 are significantly higher compared to Col-0 after ABA treatment, indicating that JMJ28 activates gene expression by H3K9me2 demethylation. Furthermore, the levels of H3K9 acetylation (H3K9ac) on RD26, ABI2 and RD29A/B are significantly decreased in jmj28, hac3-2 and jmj28/hac3-2, indicating that JMJ28 positively regulates H3K9ac mediated by GCN5. Taken together, we concluded that ABA induces gene expression by removing the repressive mark H3K9me2 and adding the active mark H3K9ac mediated by JMJ28 and GCN5, respectively.