The shoot apical meristem and cotyledons of higher plants are established during embryogenesis in the apex. Redundant CUP-SHAPED COTYLEDON 1(CUC1) and CUC2 as well as SHOOT MERISTEMLESS (STM) of Arabidopsis are required for shoot apical meristem formation and cotyledon

In higher plants, most of the above-ground part ultimately derives from small populations of mitotic cells, called the shoot apical meristem (SAM). The SAM is initially formed during embryogenesis, when the basic body architecture of a plant is established (Jürgens, 1995). Once formed, the SAM plays central roles in postembryonic shoot organ formation. The SAM generates stems, leaves, and floral organs in a set pattern while it maintains a pool of undifferentiated cells in the center (Steeves and Sussex, 1989). Thus, SAM formation during embryogenesis is a critical step to start subsequent vegetative and reproductive development. Many of the recent molecular genetic works have been focused on SAM function in postembryonic development (reviewed in Clark, 1997; Meyerowitz, 1997). However, the molecular genetic basis of SAM formation during embryogenesis is poorly understood. The embryonic SAM is formed in the apex between cotyledons in dicotyledonous plants. In Arabidopsis, the zygote undergoes stereotyped cell divisions to form the radially symmetrical embryo proper and the extraembryonic suspensor (the globular stage). By the heart stage, cotyledon primordia arise as two distinct bumps from the apical flanks of the embryo and the symmetry of the embryo shifts from radial to bilateral. As cotyledons grow and bend over the embryo apex (the bending-cotyledon stage), the SAM becomes a histologically distinct structure (Barton and Poethig, 1993). Both histological and clonal analyses suggest that the entire SAM and most of the cotyledons derive from the apical half of the globular embryo (Barton and Poethig, 1993; Scheres et al., 1994). Several Arabidopsismutants are defective only in the SAM, suggesting that at least some part of SAM formation is genetically distinct from that of cotyledons. Recessive mutations in PINHEAD(PNH; same as ZWILLE [ZLL], which was identified independently) and WUSCHEL (WUS) specifically affect SAM formation, resulting in a flat or aberrant structure at the site normally occupied by the SAM (McConnell and Barton, 1995; Laux et al., 1996; Moussian et al., 1998). These genes are suggested to be involved in organizing functional domains within the SAM. The clavata1 (clv1) and clv3mutants have an enlarged SAM, suggesting that CLV1 and CLV3 are required to limit cell populations within the SAM (Clark et al., 1995, 1996). On the other hand, several mutations that affect development of both the SAM and cotyledons have been identified, suggesting that their genetic pathways overlap. Mutations in the SHOOTMERISTEMLESS(STM) gene result in the lack of SAM and a slight fusion of the cotyledons at the base, indicating that STMis essential for embryonic SAM formation and partially required for cotyledon separation (Barton and Poethig, 1993; Clark et al., 1996; Endrizzi et al., 1996; Long and Barton, 1998). Weak alleles of stmproduce a phenotype 1563 Development 126, 1563-1570 (1999) Printed in Great Britain © The Company of Biologists Limited 1999 DEV0209