Dephosphorylation of bZIP59 by PP2A ensures appropriate shade avoidance response in Arabidopsis

Changes in light quality and quantity experienced by many shade-intolerant plants grown in close proximity lead to transcriptional reprogramming and shade avoidance syndrome (SAS). Despite the importance of phosphorylation-dependent signaling in cellular physiology, phosphorylation events during SAS are largely unknown. Here, we examined shade-regulated phosphorylation events in Arabidopsis using quantitative phosphoproteomics. We confirmed shade-induced dephosphorylation of bZIP59, a basic region/leucine zipper motif (bZIP) transcription factor. Shade treatment promotes the nuclear localization of bZIP59, which can be mimicked by mutation of the phosphorylation sites on bZIP59. Phenotypic analysis identified that bZIP59 negatively regulated shade-induced hypocotyl elongation. bZIP59 repressed the shade-induced activation of certain growth-related genes, while shade increased the DNA binding of bZIP59. Furthermore, the protein phosphatase 2A (PP2A) mediated de-phosphorylation of bZIP59. Our study characterized a previously unidentified mechanism by which the phyB-PP2A-bZIP59 regulatory module integrates shade signals and transcriptomes, broadening our knowledge of phosphorylation strategies for rapid adaptation to shade.

众多耐阴植物在相邻种植条件下所经历的亮度和光照强度变化，导致其转录重编程及避阴综合征（SAS）的发生。尽管磷酸化依赖性信号在细胞生理学中具有重要意义，但在SAS过程中的磷酸化事件却鲜有研究。本研究采用定量磷酸蛋白组学方法，考察了拟南芥中的避阴调控磷酸化事件。我们证实了避阴诱导的bZIP59（基本区域/亮氨酸拉链结构域转录因子）去磷酸化现象。避阴处理促进了bZIP59的核定位，这一过程可通过bZIP59上磷酸化位点的突变来模拟。表型分析揭示了bZIP59对避阴诱导的胚轴伸长的负调控作用。bZIP59抑制了避阴诱导的某些与生长相关的基因的激活，同时避阴增加了bZIP59的DNA结合能力。此外，蛋白磷酸酶2A（PP2A）介导了bZIP59的去磷酸化。本研究揭示了phyB-PP2A-bZIP59调控模块整合避阴信号和转录组的一种先前未知的机制，丰富了我们对快速适应避阴条件的磷酸化策略的认知。