Leaf senescence plays a critical role in a plant’s overall reproductive success due to its involvement in nutrient remobilization and allocation. However, our current understanding of the molecular mechanisms controlling leaf senescence remains limited. In this study, we show that the receptor-like kinase MALE DISCOVERER 1-INTERACTING RECEPTOR-LIKE KINASE 2 (MIK2) functions as a negative regulator of leaf senescence. We found that the SERINE-RICH ENDOGENOUS PEPTIDE 12, previously known to physically interact with MIK2, competes with SCOOP10 to regulate MIK2-dependent leaf senescence. We observed that increased expression of SCOOP10 or the application of exogenous SCOOP10 peptides accelerated leaf senescence in a MIK2-dependent manner. Conversely, SCOOP12 acted as a suppressor of MIK2-dependent leaf senescence regulation. Biochemical assays showed that SCOOP12 enhances while SCOOP10 diminishes MIK2 phosphorylation. Thus, the SCOOP12-MIK2 module might function antagonistically on SCOOP10-MIK2 signaling at late senescing stages, allowing for fine-tuned modulation of the leaf senescence process. Our study sheds light on the complex mechanisms underlying leaf senescence and provides valuable insights into the interplay between receptors, peptides, and the regulation of plant senescence.

中文翻译：

---

SCOOP10 和 SCOOP12 肽通过 MIK2 受体样激酶起作用，拮抗调节拟南芥叶片衰老


叶片衰老在植物的整体繁殖成功中起着关键作用，因为它参与养分再动员和分配。然而，我们目前对控制叶片衰老的分子机制的理解仍然有限。在这项研究中，我们表明受体样激酶 MALE DISCOVERER 1-相互作用的受体样激酶 2 （MIK2） 作为叶片衰老的负调节因子发挥作用。我们发现，以前已知与 MIK2 物理相互作用的富含丝氨酸的内源性肽 12 与 SCOOP10 竞争以调节 MIK2 依赖性叶片衰老。我们观察到 SCOOP10 表达的增加或外源 SCOOP10 肽的应用以 MIK2 依赖性方式加速叶片衰老。相反，SCOOP12 作为 MIK2 依赖性叶片衰老调节的抑制因子。生化测定显示，SCOOP12 增强而 SCOOP10 减少 MIK2 磷酸化。因此，SCOOP12-MIK2 模块可能在后期对 SCOOP10-MIK2 信号传导起拮抗作用，从而允许对叶片衰老过程进行微调调节。我们的研究阐明了叶片衰老的复杂机制，并为受体、肽和植物衰老调节之间的相互作用提供了有价值的见解。