Department of Chemistry, Seoul National University, Seoul 08826, Korea.
Plant Genomics and Breeding Institute, Seoul National University, Seoul 08826, Korea.
Plant Cell Physiol. 2022 Mar 11;63(3):326-339. doi: 10.1093/pcp/pcab178.
Leaf senescence is an active developmental process that is tightly regulated through extensive transcriptional and metabolic reprogramming events, which underlie controlled degradation and relocation of nutrients from aged or metabolically inactive leaves to young organs. The onset of leaf senescence is coordinately modulated by intrinsic aging programs and environmental conditions, such as prolonged darkness and temperature extremes. Seedlings growing under light deprivation, as often experienced in severe shading or night darkening, exhibit an accelerated senescing process, which is mediated by a complex signaling network that includes sugar starvation responses and light signaling events via the phytochrome B (phyB)-PHYTOCHROME-INTERACTING FACTOR (PIF) signaling routes. Notably, recent studies indicate that nonstressful ambient temperatures profoundly influence the onset and progression of leaf senescence in darkness, presumably mediated by the phyB-PIF4 signaling pathways. However, it is not fully understood how temperature signals regulate leaf senescence at the molecular level. Here, we demonstrated that low ambient temperatures repress the nuclear export of phyB and the nuclear phyB suppresses the transcriptional activation activity of ethylene signaling mediator ETHYLENE INSENSITIVE3 (EIN3), thus delaying leaf senescence. Accordingly, leaf senescence was insensitive to low ambient temperatures in transgenic plants overexpressing a constitutively nuclear phyB form, as observed in ein3 eil1 mutants. In contrast, leaf senescence was significantly promoted in phyB-deficient mutants under identical temperature conditions. Our data indicate that phyB coordinately integrates light and temperature cues into the EIN3-mediated ethylene signaling pathway that regulates leaf senescence under light deprivation, which would enhance plant fitness under fluctuating natural environments.
叶片衰老是一个受严格调控的主动发育过程，通过广泛的转录和代谢重编程事件来实现，这些事件是叶片中养分从衰老或代谢不活跃的叶片受控降解和转移到幼嫩器官的基础。叶片衰老的开始是由内在的衰老程序和环境条件共同调节的，如长时间的黑暗和极端温度。在光照剥夺下生长的幼苗，如在严重遮荫或夜间变暗时经常经历的情况，表现出加速衰老的过程，这是由一个复杂的信号网络介导的，包括糖饥饿反应和通过光敏色素 B（phyB）-光敏色素相互作用因子（PIF）信号途径的光信号事件。值得注意的是，最近的研究表明，非胁迫性环境温度深刻地影响黑暗中叶片衰老的开始和进程，可能是通过 phyB-PIF4 信号通路介导的。然而，温度信号如何在分子水平上调节叶片衰老还不完全清楚。在这里，我们证明了低温抑制 phyB 的核输出，核内 phyB 抑制乙烯信号介质 ETHYLENE INSENSITIVE3（EIN3）的转录激活活性，从而延缓叶片衰老。因此，在过表达组成型核 phyB 形式的转基因植物中，叶片衰老对低温不敏感，如在 ein3 eil1 突变体中观察到的那样。相比之下，在相同温度条件下，phyB 缺陷突变体中的叶片衰老显著促进。我们的数据表明，phyB 将光和温度线索协调整合到 EIN3 介导的乙烯信号通路中，该通路调节光照剥夺下的叶片衰老，这将增强植物在波动的自然环境中的适应性。
