Epigenetic modifications play vital roles in many biological processes. Flower senescence involves epigenetic factors that influence the chromatin state and gene expression. However, the molecular mechanism underlying the role of histone deacetylation in regulating flower senescence has not been elucidated. Here, we demonstrate that histone deacetylation is involved in flower senescence by fine-tuning reactive oxygen species (ROS) homeostasis in rose (Rosa hybrida). Our data reveal that the histone lysine deacetyltransferase RhHDA15 inhibits ROS accumulation and petal senescence by downregulating the expression of NADPH OXIDASE/RESPIRATORY BURST OXIDASE HOMOLOG (RhRboh) genes. Furthermore, the transcription factor RELATED TO ABI3/VP1 2 (RhRAV2) recruits RhHDA15 and the co-repressor TOPLESS (RhTPL) to suppress flower senescence by reducing H3 lysine 9 acetylation (H3K9ac) at the RhRbohA1/2 promoter and thus directly inhibiting precocious RhRbohA1/2 expression. Our work sheds light on an epigenetic mechanism in which histone deacetylation plays a crucial role in controlling petal senescence by precisely fine-tuning ROS homeostasis, providing insights into the regulatory network of organ senescence.

中文翻译：

---

组蛋白脱乙酰酶 RhHDA15 通过表观遗传调节玫瑰中的活性氧稳态来抑制花瓣衰老


表观遗传修饰在许多生物过程中起着至关重要的作用。花衰老涉及影响染色质状态和基因表达的表观遗传因素。然而，组蛋白脱乙酰化在调节花衰老中作用的分子机制尚未阐明。在这里，我们通过微调玫瑰 （Rosa hybrida） 中的活性氧 （ROS） 稳态证明组蛋白脱乙酰化与花衰老有关。我们的数据显示，组蛋白赖氨酸脱乙酰转移酶 RhHDA15 通过下调 NADPH 氧化酶/呼吸爆发氧化酶同源物 （RhRboh） 基因的表达来抑制 ROS 积累和花瓣衰老。此外，与 ABI3/VP1 2 相关的转录因子 （RhRAV2） 通过减少 RhRbohA1/2 启动子处的 H3 赖氨酸 9 乙酰化 （H3K9ac） 来募集 RhHDA15 和共阻遏物 TOPLESS （RhTPL），从而直接抑制性早熟 RhRbohA1/2 表达，从而抑制花衰老。我们的工作阐明了一种表观遗传机制，其中组蛋白脱乙酰化通过精确微调 ROS 稳态在控制花瓣衰老中起关键作用，为器官衰老的调控网络提供了见解。