摘要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 phys-ically 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-depen dent 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 antag-onistically 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.