Abstract

SHOOT MERISTEMLESS ( STM ), a homeobox transcription factor, functions to maintain shoot apical meristem (SAM) and floral meristem (FM) activity. Carpel formation is abolished in stm mutant flowers, but this phenotype can be partially restored by compromising the function of SERRATE (SE), the core component in miRNA formation. However, whether and how SE functions in meristem maintenance and flower development remains mysterious. Here, we show that the partial loss-of-function mutant of SE ( se-1 ) shows additional floral organs and enlarged SAM sizes, and could restore FM activity in the stm mutant. We further demonstrate that SE represses the expression of STM-targeted KNOTTED-LIKE FROM ARABIDOPSIS THALIANA 2 ( KNAT2 ) through miR171c-5p, thereby inhibiting the expression of ISOPENTENYL TRANSFERASE 7 ( IPT7 ), which is activated by STM and is required for cytokinin biosynthesis. IPT7 can also be repressed by SE through the miR164c–CUP-SHAPED COTYLEDON 1/2 (CUC1/2)–KNAT2 regulatory module. Thus, FM activity promoted by restored cytokinin signaling could restore carpel formation in the se stm double mutant. The antagonistic regulation between SE and STM for FM maintenance ensures proper carpel development in Arabidopsis.