ABSTRACT

Plants have evolved many leucine-rich repeat receptor-like kinases (LRR-RLKs) that control all aspects of plant life in a kinase-dependent or -independent manner. DROOPY LEAF1 (DPY1), which is a subfamily II LRR-RLK authentic kinase, controls leaf droopiness by negatively regulating early brassinosteroid (BR) signaling in foxtail millet. In this study, we proved that overexpressing kinase-inactive DPY1 does not rescue the droopy leaf phenotype of dpy1 plants because the mutated DPY1 cannot repress BR signaling, suggesting that kinase activity is required for DPY1 to control BR signaling. Moreover, seven DPY1 sites potentially transphosphorylated by SiBAK1 were identified as crucial for DPY1 activation. These findings highlight the importance of kinase activity for the functionality of DPY1.

摘要

植物已经进化出许多富含亮氨酸的重复受体样激酶 (LRR-RLK)，它们以激酶依赖性或非依赖性方式控制植物生命的各个方面。DROOPY LEAF1 (DPY1) 是一种亚家族 II LRR-RLK 真正的激酶，通过负调控谷子早期油菜素内酯 (BR) 信号来控制叶片下垂。在这项研究中，我们证明过表达激酶失活的 DPY1 并不能挽救dpy1植物的下垂叶片表型，因为突变的 DPY1 不能抑制 BR 信号传导，这表明 DPY1 需要激酶活性来控制 BR 信号传导。此外，七个可能被 SiBAK1 转磷酸化的 DPY1 位点被确定为对 DPY1 激活至关重要。这些发现强调了激酶活性对 DPY1 功能的重要性。