Drought is one of the major threats to forest productivity. Oxidation stress is common in drought-stressed plants, and plants need to maintain normal life activities through complex reactive oxygen scavenging mechanisms. However, the molecular links between epigenetics, oxidation stress, and drought in poplar (Populus) remain poorly understood. Here, we found that Populus plants overexpressing PtrMYB94, which encodes a R2R3 MYB transcription factor that regulates the ABA signaling pathway, displayed increased tolerance to extreme drought stress via up-regulation of embryogenic cell phosphoprotein 44 (PtrECPP44) expression. Further investigation revealed that PtrMYB94 could recruit the histone deacetylases PtrHDA907/908 to the promoter of PtrECPP44 and decrease acetylation at lysine residues 9, 14 and 27 of histone H3, leading to relatively low transcriptional expression levels under normal conditions. Drought induced the expression of PtrMYB94 while preventing interaction of PtrMYB94 with PtrHDA907/908, which relaxed the chromatin structure and facilitated the binding of RNA polymerase II to the PtrECPP44 promoter. The upregulation of PtrECPP44 helped poplar alleviate oxidative damage and maintain normal cell activities. This study establishes a PtrMYB94-PtrECPP44 transcriptional regulatory module modified by PtrHDA907/908 in modulating drought-induced oxidative stress recovery. Therefore, our study reveals a oxidative regulatory mechanism in response to drought stress and provides insights into molecular breeding for stress resistance in poplar.

中文翻译：

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转录因子 MYB94 和组蛋白脱乙酰酶 HDA907/908 的解离减轻杨树的氧化损伤


干旱是森林生产力的主要威胁之一。氧化应激在干旱胁迫植物中很常见，植物需要通过复杂的活性氧清除机制来维持正常的生命活动。然而，杨树表观遗传学、氧化应激和干旱之间的分子联系仍然知之甚少。在这里，我们发现过表达 PtrMYB94（编码调节 ABA 信号通路的 R2R3 MYB 转录因子）的杨属植物通过上调胚性细胞磷蛋白 44 (PtrECPP44) 表达而表现出对极端干旱胁迫的耐受性增强。进一步研究表明，PtrMYB94 可以将组蛋白脱乙酰酶 PtrHDA907/908 招募到 PtrECPP44 的启动子上，并降低组蛋白 H3 赖氨酸残基 9、14 和 27 的乙酰化，导致正常条件下相对较低的转录表达水平。干旱诱导 PtrMYB94 的表达，同时阻止 PtrMYB94 与 PtrHDA907/908 的相互作用，从而松弛染色质结构并促进 RNA 聚合酶 II 与 PtrECPP44 启动子的结合。 PtrECPP44的上调有助于杨减轻氧化损伤并维持正常的细胞活性。本研究建立了经 PtrHDA907/908 修饰的 PtrMYB94-PtrECPP44 转录调控模块，用于调节干旱诱导的氧化应激恢复。因此，我们的研究揭示了响应干旱胁迫的氧化调节机制，并为杨树抗逆性分子育种提供了见解。