背景回顾：Leaf senescence is an important developmental process in plants’ life cycle and has a significant impact on agriculture. As an adaptive mechanism, when facing harsh environmental conditions, monocarpic plants often initiate leaf senescence early to ensure a complete life cycle. Upon initiation, the senescence process is fine-tuned through the coordination of both positive and negative regulators. 

主要发现：Here we report a small secreted peptide, CLAVATA3/ESR-RELATED (CLE) 14, which functions in suppressing leaf senescence through regulating ROS homeostasis in Arabidopsis. 

结果1-CLE14在叶片中的诱导表达模式：Expression of the CLE14-encoding gene in leaves was significantly induced by age, high salinity, abscisic acid (ABA), salicylic acid (SA) and jasmonic acid (JA).

结果2-CLE14敲除与过表达或外施处理表型：CLE14 knock-out plants displayed accelerated progression of both natural and salinity-induced leaf senescence. On the other hand, increased CLE14 expression or treatments with synthetic CLE14 peptides delayed senescence. CLE14 peptide treatments also caused delay in ABA-induced senescence in detached leaves. 

结果3-CLE14与ROS：Further analysis showed that CLE14 gain-of-function led to reduced ROS levels in leaves, where higher expression of ROS scavenging genes were detected. 

结果4-CLE14-JUB1-ROS清除：Moreover, CLE14 signaling resulted in transcriptional activation of JUB1, a NAC family transcription factor previously identified as a negative regulator of senescence. 

结果5-CLE14-JUB1-ROS清除-延缓衰老：Notably, the function of CLE14 peptides was JUB1-dependent in delaying leaf senescence, reducing H2O2 level, and activating ROS scavenging genes. 

结论：We propose that small peptide CLE14 serves as a novel “brake signal” in regulating age-dependent and stress-induced leaf senescence through JUB1-mediated ROS scavenging.

 摘 要 

叶片衰老是植物生命周期中一个重要的发育进程，对于农业来说具有非常重要的影响。作为一种适应机制，当面临恶劣的环境条件时，一次结实的植物通常会提前开始叶片衰老，以确保生命周期的完整。一旦开始，衰老就会由正向和负向调控因子的协同作用精细调节。本文中，作者报道了拟南芥中一个小的分泌多肽CLE14通过调控活性氧物质ROS的内稳态，抑制叶片的衰老。叶片中CLE14基因的表达受到年龄、高盐、脱落酸、水杨酸和茉莉酸的显著诱导。CLE14敲除株系的叶片自然衰老和盐诱导的衰老进程明显加快。换句话说，CLE14表达量的增加或是合成CLE14多肽的处理会延迟叶片衰老。CLE14多肽的处理还会延迟离体叶片由ABA诱导的叶片衰老。进一步的分析发现CLE14功能获得的植株叶片ROS水平明显降低，其中ROS清除基因的表达明显增强。此外，CLE14信号转导会激活一个NAC转录因子JUB1的转录激活，该基因是衰老的一个负调控因子。有趣的是，CLE14多肽在延迟叶片发育、降低过氧化氢水平以及激活ROS清除基因等方面的功能依赖于JUB1。因此，作者认为小肽CLE14作为一个新的“刹车信号”，通过JUB1介导的ROS清除来调控年龄依赖性和胁迫诱导的叶片衰老。