Oxygen deficiency (hypoxia) occurs naturally in many developing plant tissues but can become a major threat during acute flooding stress. Consequently, plants as aerobic organisms must rapidly acclimate to hypoxia and the associated energy crisis to ensure cellular and ultimately organismal survival. In plants, oxygen sensing is tightly linked with oxygen-controlled protein stability of group VII ETHYLENE-RESPONSE FACTORs (ERFVII), which, when stabilized under hypoxia, act as key transcriptional regulators of hypoxia-responsive genes (HRGs). Multiple signaling pathways feed into hypoxia signaling to fine-tune cellular decision-making under stress. First, ATP shortage upon hypoxia directly affects the energy status and adjusts anaerobic metabolism. Secondly, altered redox homeostasis leads to reactive oxygen and nitrogen species (ROS and RNS) accumulation, evoking signaling and oxidative stress acclimation. Finally, the phytohormone ethylene promotes hypoxia signaling to improve acute stress acclimation, while hypoxia signaling in turn can alter ethylene, auxin, abscisic acid, salicylic acid, and jasmonate signaling to guide development and stress responses. In this Update, we summarize the current knowledge on how energy, redox, and hormone signaling pathways are induced under hypoxia and subsequently integrated at the molecular level to ensure stress-tailored cellular responses. We show that some HRGs are responsive to changes in redox, energy, and ethylene independently of the oxygen status, and we propose an updated HRG list that is more representative for hypoxia marker gene expression. We discuss the synergistic effects of hypoxia, energy, redox, and hormone signaling and their phenotypic consequences in the context of both environmental and developmental hypoxia.

中文翻译：

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缺氧信号与能量、氧化还原和激素线索的机制整合


缺氧（缺氧）自然发生在许多发育中的植物组织中，但在急性洪水胁迫期间可能成为主要威胁。因此，植物作为好氧生物必须迅速适应缺氧和相关的能量危机，以确保细胞和最终有机体的生存。在植物中，氧感应与 VII 组乙烯反应因子 （ERFVII） 的氧控制蛋白质稳定性密切相关，当在缺氧下稳定时，它充当缺氧反应基因 （HRG） 的关键转录调节因子。多个信号通路馈入缺氧信号传导，以微调压力下的细胞决策。首先，缺氧时 ATP 短缺直接影响能量状态并调整厌氧代谢。其次，改变的氧化还原稳态导致活性氧和氮物质 （ROS 和 RNS） 积累，诱发信号传导和氧化应激驯化。最后，植物激素乙烯促进缺氧信号传导以改善急性应激适应，而缺氧信号又可以改变乙烯、生长素、脱落酸、水杨酸和茉莉酸酯信号传导，以指导发育和应激反应。在此更新中，我们总结了当前关于如何在缺氧下诱导能量、氧化还原和激素信号通路，并随后在分子水平上整合以确保针对应激的细胞反应的知识。我们表明，一些 HRG 对氧化还原、能量和乙烯的变化有反应，而与氧状态无关，我们提出了一个更新的 HRG 列表，该列表更能代表缺氧标志物基因表达。我们讨论了缺氧、能量、氧化还原和激素信号传导的协同作用及其在环境和发育缺氧背景下的表型后果。