MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China; Guangdong Provincial Key Laboratory of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China.
MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China; Guangdong Provincial Key Laboratory of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China.
Plant Sci. 2023 Nov;336:111859. doi: 10.1016/j.plantsci.2023.111859. Epub 2023 Sep 4.
In plants, leaf senescence is regulated by several factors, including age and carbon starvation. The molecular mechanism of age-regulated developmental leaf senescence differs from that of carbon starvation-induced senescence. Salicylic acid (SA) and Nonexpressor of pathogenesis-related genes 1 (NPR1) play important roles in promoting developmental leaf senescence. However, the relationship between SA signaling and carbon starvation-induced leaf senescence is not currently well understood. Here, we used Arabidopsis thaliana as material and found that carbon starvation-induced leaf senescence was accelerated in the SA dihydroxylase mutants s3hs5h compared to the Columbia ecotype (Col). Exogenous SA treatment significantly promoted carbon starvation-induced leaf senescence, especially in NPR1-GFP. Increasing the endogenous SA and overexpression of NPR1 inhibited carbon starvation-induced autophagy. However, mutation of NPR1 delayed carbon starvation-induced leaf senescence, increased autophagosome production and accelerated autophagic degradation of the Neighbor of BRCA1 gene 1 (NBR1). In conclusion, SA promotes carbon starvation-induced leaf senescence by inhibiting autophagy via NPR1.
在植物中，叶片衰老受多种因素的调控，包括年龄和碳饥饿。年龄调控的发育性叶片衰老的分子机制与碳饥饿诱导的衰老不同。水杨酸（SA）和非表达病程相关基因 1（NPR1）在促进发育性叶片衰老中发挥重要作用。然而，SA 信号与碳饥饿诱导的叶片衰老之间的关系目前还不是很清楚。在这里，我们以拟南芥为材料，发现与哥伦比亚生态型（Col）相比，碳饥饿诱导的叶片衰老在水杨酸二羟化酶突变体 s3hs5h 中加速。外源 SA 处理显著促进了碳饥饿诱导的叶片衰老，特别是在 NPR1-GFP 中。增加内源性 SA 和过表达 NPR1 抑制了碳饥饿诱导的自噬。然而，突变 NPR1 延迟了碳饥饿诱导的叶片衰老，增加了自噬体的产生，并加速了 BRCA1 基因 1（NBR1）的自噬性降解。总之，SA 通过 NPR1 抑制自噬来促进碳饥饿诱导的叶片衰老。
