Shanghai Key Laboratory of Bio-Energy Crops, School of Life Sciences, Shanghai University, Shanghai, China.
Department of Agronomy, University of Almeria, Almeria, Spain.
Physiol Plant. 2024 Jul-Aug;176(4):e14490. doi: 10.1111/ppl.14490.
Seed germination and dormancy represent critical phases in the life cycle of plants, tightly regulated by endogenous phytochrome levels and environment signals. High temperatures (HT) induce the overaccumulation of reactive oxygen species (ROS) and increase abscisic acid (ABA), thereby inhibiting seed germination. Our previous findings showed that HT induced the burst of reactive nitrogen species (RNS), increasing the S-nitrosylation modification of HFR1, which effectively blocks seed germination. Importantly, stabilizing HFR1 has been shown to significantly mitigate the inhibitory effect of HT on seed germination. In this study, we reported that HT increased the protein abundance of ABI4, a crucial component in ABA signaling, which in turn activates the expression of RbohD while suppressing the expression of VTC2. This leads to the rapid generation of ROS, thereby inhibiting seed germination. Consistently, the seed germination of abi4 mutant showed insensitivity to HT with lower ROS level during seed germination, whereas transgenic lines overexpressing ABI4 showed reduced germination rates accompanied by elevated ROS levels. Furthermore, we noted that HFR1 interacts with ABI4 to sequester its activity under normal conditions. However, HT-induced ROS triggered the degradation of HFR1, consequently releasing ABI4 activity. This activation of ABI4 promotes RbohD expression, culminating in a ROS burst that suppresses seed germination. Thus, our study unveils a novel function for ABI4 in regulating ROS level and seed germination under HT stress. Throughout this process, HFR1 plays a critical role in restraining ABI4 activity to maintain an optimal endogenous ROS level, thereby ensuring seed germination under favorable environmental conditions.
种子萌发和休眠是植物生命周期中的关键阶段，受内源光敏色素水平和环境信号的严格调控。高温（HT）诱导活性氧（ROS）的过度积累，并增加脱落酸（ABA），从而抑制种子萌发。我们之前的研究结果表明，HT 诱导活性氮物种（RNS）的爆发，增加 HFR1 的 S-亚硝基化修饰，有效地阻止种子萌发。重要的是，稳定 HFR1 已被证明能显著减轻 HT 对种子萌发的抑制作用。在这项研究中，我们报告了 HT 增加了 ABA 信号中关键成分 ABI4 的蛋白丰度，从而激活 RbohD 的表达，同时抑制 VTC2 的表达。这导致 ROS 的快速产生，从而抑制种子萌发。一致地，abi4 突变体的种子萌发对 HT 不敏感，在种子萌发期间 ROS 水平较低，而过表达 ABI4 的转基因系表现出较低的萌发率和较高的 ROS 水平。此外，我们注意到 HFR1 与 ABI4 相互作用，在正常条件下使其活性被隔离。然而，HT 诱导的 ROS 触发了 HFR1 的降解，从而释放了 ABI4 的活性。ABI4 的这种激活促进了 RbohD 的表达，最终导致 ROS 的爆发，从而抑制了种子的萌发。因此，我们的研究揭示了 ABI4 在 HT 胁迫下调节 ROS 水平和种子萌发的新功能。在整个过程中，HFR1 起着关键作用，它可以抑制 ABI4 的活性，以维持最佳的内源性 ROS 水平，从而确保在有利的环境条件下种子的萌发。
