SP3 and DEP1 Orchestrate Panicle Architecture by Jointly Regulating APO2 Expression in Rice

Panicle architecture is largely determined by meristem activity. This previous study shows that DNA binding with one finger (Dof) transcription factor Short Panicle 3 (SP3) regulates panicle architecture. However, the molecular mechanisms of SP3 controlling panicle architecture remain largely unknown. Here, SP3 is shown to enhance inflorescence meristem (IM) activity. Histological analysis shows that IM size rather than the timing of the meristem transition significantly reduces in SP3 mutants. Several assays reveal that SP3 interacts with the C-terminal cysteine-rich domain of DENSE AND ERECT PANICLE1 (DEP1), a class C Gγ subunit, thereby regulating its plasma membrane-nucleus shuttle. SP3 directly binds to the cis element (A/T)AAAG located within the -561 to -517 bp region upstream of the ABERRANT PANICLE ORGANIZATION2 (APO2) promoter and activates APO2 expression, a positive regulator of panicle size. Genetic analysis indicates that APO2 functions downstream of SP3 to promote panicle branching. Additionally, loss of function of DEP1 increases APO2 expression and spikelet density. Transcriptional activity assays show that the interaction between DEP1 and SP3 suppresses SP3-mediated activation on APO2. Altogether, this study uncovers a transcriptional regulatory mechanism involving SP3 and DEP1 in controlling APO2 expression, offering new insights into the genetic network underlying rice panicle development.