Angiosperm leaves show extensive shape diversity and are broadly divided into two forms; simple leaves with intact lamina and compound leaves with lamina dissected into leaflets. The mechanistic basis of margin dissection and leaflet initiation has been inferred primarily by analysing compound-leaf architecture, and thus whether the intact lamina of simple leaves has the potential to initiate leaflets upon endogenous gene inactivation remains unclear. Here, we show that the CINCINNATA-like TEOSINTE BRANCHED1, CYCLOIDEA, PROLIFERATING CELL FACTORS (CIN-TCP) transcription factors activate the class II KNOTTED1-LIKE (KNOX-II) genes and the CIN-TCP and KNOX-II proteins together redundantly suppress leaflet initiation in simple leaves. Simultaneous downregulation of CIN-TCP and KNOX-II in Arabidopsis leads to the reactivation of the stemness genes KNOX-I and CUPSHAPED COTYLEDON (CUC) and triggers ectopic organogenesis, eventually converting the simple lamina to a super-compound form that appears to initiate leaflets indefinitely. Thus, a conserved developmental mechanism promotes simple leaf architecture in which CIN-TCP–KNOX-II forms a strong differentiation module that suppresses the KNOX-I-CUC network and leaflet initiation.

被子植物的叶子表现出广泛的形状多样性，大致分为两种形式；带完整叶片的单叶和带叶片的复叶解剖成小叶。边缘解剖和小叶启动的机制基础主要通过分析复合叶结构来推断，因此简单叶的完整叶片是否具有在内源基因失活后启动小叶的潜力仍不清楚。在这里，我们表明 CINCINNATA 样 TEOSINTE BRANCHED1、CYCLOIDEA、增殖细胞因子 (CIN-TCP) 转录因子激活 II 类KNOTTED1-LIKE ( KNOX-II ) 基因和 CIN-TCP 和 KNOX-II 蛋白一起冗余抑制单叶中的传单起始。CIN-TCP 和 KNOX-II 的同时下调拟南芥导致干性基因KNOX-I和CUPSHAPED COTYLEDON ( CUC ) 的重新激活并触发异位器官发生，最终将简单的叶片转化为超级复合形式，似乎可以无限期地启动小叶。因此，一种保守的发育机制促进了简单的叶结构，其中 CIN-TCP-KNOX-II 形成了一个强大的分化模块，抑制了 KNOX-I-CUC 网络和小叶的启动。