JAG modulates sepal flatness by regulating cell growth direction, interacts with AS2, and is antagonized by TCP24

Flat plant organs are crucial for optimal organ functionality. Polarity establishment and growth coordination between tissues are key factors in maintaining organ flatness. Ectopic ASYMMETRIC LEAVES2 (AS2) expression in the as2-7D mutant has been shown to disrupt growth across cell layers, leading to epidermal buckling in sepals. However, the detailed molecular mechanism remains unclear. Here, we show that mutation of the JAGGED (JAG) gene suppresses buckling of the as2-7D sepal epidermis. Cellular growth analysis reveals that the jag mutant suppresses the sepal epidermal buckling phenotype by altering cellular growth directions to be more parallel with the proximal-distal direction. On the molecular level, JAG physically interacts with AS2. TEOSINTE BRANCHED 1, CYCLOIDEA, AND PCF FAMILY 24 (TCP24) antagonizes JAG in sepal morphogenesis by repressing JAG transcription and inhibiting the AS2-JAG protein interaction. Our study uncovers a complex molecular network involving AS2, JAG, and TCP24 that is critical for generating flat plant organs.