Department of Chemistry, Seoul National University, Seoul, 08826, Republic of Korea.
Plant Genomics and Breeding Institute, Seoul National University, Seoul, 08826, Republic of Korea.
Nat Commun. 2019 Apr 12;10(1):1713. doi: 10.1038/s41467-019-09417-1.
Unlike activation of target genes in response to abscisic acid (ABA), how MYB96 transcription factor represses ABA-repressible genes to further enhance ABA responses remains unknown. Here, we show MYB96 interacts with the histone modifier HDA15 to suppress negative regulators of early ABA signaling. The MYB96-HDA15 complex co-binds to the promoters of a subset of RHO GTPASE OF PLANTS (ROP) genes, ROP6, ROP10, and ROP11, and represses their expression by removing acetyl groups of histone H3 and H4 from the cognate regions, particularly in the presence of ABA. In support, HDA15-deficient mutants display reduced ABA sensitivity and are susceptible to drought stress with derepression of the ROP genes, as observed in the myb96-1 mutant. Biochemical and genetic analyses show that MYB96 and HDA15 are interdependent in the regulation of ROP suppression. Thus, MYB96 confers maximal ABA sensitivity by regulating both positive and negative regulators of ABA signaling through distinctive molecular mechanisms.
与响应脱落酸 (ABA) 激活靶基因不同，MYB96 转录因子如何抑制 ABA 抑制基因以进一步增强 ABA 反应尚不清楚。在这里，我们显示 MYB96 与组蛋白修饰酶 HDA15 相互作用，以抑制早期 ABA 信号转导的负调控因子。MYB96-HDA15 复合物共同结合到一组 RHO GTPASE OF PLANTS (ROP) 基因、ROP6、ROP10 和 ROP11 的启动子上，并通过从同源区域去除组蛋白 H3 和 H4 的乙酰基来抑制它们的表达，特别是在存在 ABA 的情况下。支持的是，HDA15 缺陷突变体表现出降低的 ABA 敏感性，并容易受到干旱胁迫，ROP 基因的表达被解除抑制，如在 myb96-1 突变体中观察到的那样。生化和遗传分析表明，MYB96 和 HDA15 在 ROP 抑制的调节中是相互依赖的。因此，MYB96 通过调节 ABA 信号转导的正调节剂和负调节剂，通过独特的分子机制赋予最大的 ABA 敏感性。
