Ministry of Education Key Laboratory of Molecular and Cellular Biology, Hebei Research Center of the Basic Discipline of Cell Biology, Hebei Collaboration Innovation Center for Cell Signaling and Environmental Adaptation, Hebei Key Laboratory of Molecular and Cellular Biology, College of Life Sciences, Hebei Normal University, Shijiazhuang, 050024, China.
College of Chemical Engineering, Shijiazhuang University, Shijiazhuang, 050035, China.
J Integr Plant Biol. 2024 Jun;66(6):1126-1147. doi: 10.1111/jipb.13659. Epub 2024 Apr 17.
Most mechanistic details of chronologically ordered regulation of leaf senescence are unknown. Regulatory networks centered on AtWRKY53 are crucial for orchestrating and integrating various senescence-related signals. Notably, AtWRKY53 binds to its own promoter and represses transcription of AtWRKY53, but the biological significance and mechanism underlying this self-repression remain unclear. In this study, we identified the VQ motif-containing protein AtVQ25 as a cooperator of AtWRKY53. The expression level of AtVQ25 peaked at mature stage and was specifically repressed after the onset of leaf senescence. AtVQ25-overexpressing plants and atvq25 mutants displayed precocious and delayed leaf senescence, respectively. Importantly, we identified AtWRKY53 as an interacting partner of AtVQ25. We determined that interaction between AtVQ25 and AtWRKY53 prevented AtWRKY53 from binding to W-box elements on the AtWRKY53 promoter and thus counteracted the self-repression of AtWRKY53. In addition, our RNA-sequencing data revealed that the AtVQ25-AtWRKY53 module is related to the salicylic acid (SA) pathway. Precocious leaf senescence and SA-induced leaf senescence in AtVQ25-overexpressing lines were inhibited by an SA pathway mutant, atsid2, and NahG transgenic plants; AtVQ25-overexpressing/atwrky53 plants were also insensitive to SA-induced leaf senescence. Collectively, we demonstrated that AtVQ25 directly attenuates the self-repression of AtWRKY53 during the onset of leaf senescence, which is substantially helpful for understanding the timing of leaf senescence onset modulated by AtWRKY53.
叶片衰老的时序调控的大多数机制细节尚不清楚。以 AtWRKY53 为中心的调控网络对于协调和整合各种与衰老相关的信号至关重要。值得注意的是,AtWRKY53 结合到其自身的启动子并抑制 AtWRKY53 的转录,但这种自我抑制的生物学意义和机制尚不清楚。在本研究中,我们鉴定了含有 VQ 基序的蛋白 AtVQ25 是 AtWRKY53 的协同因子。AtVQ25 的表达水平在成熟阶段达到峰值,并在叶片衰老开始后特异性受到抑制。过表达 AtVQ25 的植株和 atvq25 突变体分别表现出过早和延迟的叶片衰老。重要的是,我们鉴定了 AtWRKY53 是 AtVQ25 的相互作用伙伴。我们确定 AtVQ25 和 AtWRKY53 之间的相互作用阻止了 AtWRKY53 结合到 AtWRKY53 启动子上的 W 框元件,从而抵消了 AtWRKY53 的自我抑制。此外,我们的 RNA-seq 数据表明,AtVQ25-AtWRKY53 模块与水杨酸(SA)途径有关。在过表达 AtVQ25 的系中,SA 诱导的叶片衰老和提前衰老被 SA 途径突变体 atsid2 和 NahG 转基因植物抑制;AtVQ25 过表达/atwrky53 植株对 SA 诱导的叶片衰老也不敏感。总的来说,我们证明了 AtVQ25 在叶片衰老开始时直接减弱了 AtWRKY53 的自我抑制,这对于理解 AtWRKY53 调控的叶片衰老开始的时间具有重要意义。