Abstract
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 H2O2 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.
This study discovers that the small secreted peptide CLE14 suppresses leaf senescence by modulating ROS accumulation in Arabidopsis. The regulation of age-dependent and stress-induced leaf senescence by CLE14 requires the function of the NAC transcription factor JUB1. The CLE14-JUB1-ROS signaling module serves as a braking mechanism in the form of a negative feedback loop to prevent precocious senescence under normal or stressed conditions.