Leaf senescence is an important developmental process in the plant life cycle and has a significant impact on agriculture. When facing harsh environmental conditions, monocarpic plants often initiate early leaf senescence as an adaptive mechanism to ensure a complete life cycle. Upon initiation, the senescence process is fine-tuned through the coordination of both positive and negative regulators. Here, we report that the small secreted peptide CLAVATA3/ESR-RELATED 14 (CLE14) functions in the suppression of leaf senescence by regulating ROS homeostasis in Arabidopsis. Expression of the CLE14-encoding gene in leaves was significantly induced by age, high salinity, abscisic acid (ABA), salicylic acid, and jasmonic acid. CLE14 knockout plants displayed accelerated progression of both natural and salinity-induced leaf senescence, whereas increased CLE14 expression or treatments with synthetic CLE14 peptides delayed senescence. CLE14 peptide treatments also delayed ABA-induced senescence in detached leaves. Further analysis showed that overexpression of CLE14 led to reduced ROS levels in leaves, where higher expression of ROS scavenging genes was detected. Moreover, CLE14 signaling resulted in transcriptional activation of JUB1, a NAC family transcription factor previously identified as a negative regulator of senescence. Notably, the delay of leaf senescence, reduction in H_{2O2 level, and activation of ROS scavenging genes by} CLE14 peptides were dependent on JUB1. Collectively, these results suggest that the small peptide CLE14 serves as a novel “brake signal” to regulate age-dependent and stress-induced leaf senescence through JUB1-mediated ROS scavenging.

叶片衰老是植物生命周期中的一个重要发育过程，对农业有着重要的影响。当面临恶劣的环境条件时，单果植物通常会启动早期叶片衰老作为确保完整生命周期的适应机制。启动后，衰老过程通过正负调节器的协调进行微调。在这里，我们报告了小分泌肽 CLAVATA3/ESR-RELATED 14 (CLE14) 通过调节拟南芥中的 ROS 稳态来抑制叶片衰老。叶片中 CLE14 编码基因的表达受年龄、高盐度、脱落酸 (ABA)、水杨酸和茉莉酸显着诱导。CLE14基因敲除植物表现出自然和盐度诱导的叶片衰老的加速进展，而增加CLE14表达或用合成 CLE14 肽处理延迟衰老。CLE14 肽处理还延迟了离体叶片中 ABA 诱导的衰老。进一步分析表明，CLE14 的过表达导致叶片中 ROS 水平降低，其中检测到 ROS 清除基因的更高表达。此外，CLE14 信号导致 JUB1 的转录激活，JUB1是一种 NAC 家族转录因子，之前被确定为衰老的负调节因子。值得注意的是，叶片衰老的延迟、H _{2O2 水平的降低以及 ROS 清除基因的激活}CLE14 肽依赖于 JUB1。总的来说，这些结果表明，小肽 CLE14 作为一种新的“制动信号”，通过 JUB1 介导的 ROS 清除来调节年龄依赖性和胁迫诱导的叶片衰老。