Rice SINA E3 ligases dichotomously control ERECTA1 ubiquitination and stability to regulate panicle morphogenesis and grain yield

Abstract

Rice panicle architecture affects grain number per panicle and therefore determines grain yield. The receptor-like kinase OsER1 regulates panicle development by perceiving extracellular small peptide ligands; however, how activated OsER1 fine-tunes panicle morphogenesis remains unclear. This study reveals that members of the conserved SEVEN IN ABSENTIA OF RICE (SINAR) E3 ubiquitin ligase family regulate rice spikelet number in either synergistic or antagonistic manners by modulating the ubiquitination and stability of OsER1. Notably, SINAR1 and SINAR6 reduce the ubiquitination activity of SINAR2/3/4/5 through heterodimer formation, acting as a molecular brake to protect OsER1 from vacuolar degradation. These findings identify SINAR1 and SINAR6 as key components of a negative feedback mechanism that ensures optimal OsER1 signaling and shapes panicle architecture. Targeted suppression of SINAR1 and SINAR6 markedly enhances grain yield by promoting OsER1 degradation, demonstrating that attenuation of OsER1-mediated developmental signaling-while maintaining its function-optimizes rice panicle architecture without compromising spikelet fertility. Together, our findings reveal an antagonistic, ligase-mediated regulatory mechanism that maintains receptor homeostasis and provide a strategy to enhance rice yield through manipulation of dichotomous SINA E3 ligases.

Keywords: OsER1; SINARs; antagonistic ligases; panicle architecture; rice.