SCOOP10 And SCOOP12 Peptides Act Through MIK2 Receptor-Like Kinase to Antagonistically Regulate Arabidopsis Leaf Senescence.

Abstract

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 demonstrate that the receptor-like kinase MALE DISCOVERER 1-INTERACTING RECEPTOR-LIKE KINASE 2 (MIK2) functions as a negative regulator of leaf senescence. We report that the SERINE-RICH ENDOGENOUS PEPTIDE 12, previously known to physically interact with MIK2, competes with SCOOP10 to control MIK2-dependent senescence regulatory mechanisms. 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 senescence regulation. We also found that SCOOP12 enhanced while SCOOP10 diminished 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 research 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.