Plant Meristems: What You See Is What You Get?

The shoot apical meristem (SAM) is the ultimate source of all plant shoot cells. Continuous cell production in the meristem displaces cells towards the meristem periphery, where they organize into organ primordia. As cells exit the central zone, which contains the stem cells of the shoot, and move through the flanks to the primordia, their identity and behaviour changes: Cells in the centre have indeterminate stem cell identity, whereas cells in the periphery become determinate in the course of organ initiation. Proliferation rates are low at the centre, but increase towards its flanks and are highest in organ primordia. Genetic analysis has identified an interacting network of genes required for meristem function in plants. This network can be summarized in a simplified model in which the CLAVATA1–3 (CLV1–3) and the WUSCHEL (WUS) and SHOOTMERISTEM-LESS (STM) genes interact in a negative feedback loop to restrict stem cell numbers [1–3]. In this model, STM is required in the SAM to maintain the indeterminate state, whereas WUS is needed to maintain stem cells. CLV3 is expressed in the central zone of the SAM in the outermost L1 and L2 cell layers (Figure 1). It encodes a small polypeptide that is delivered to the apoplastic space where it moves between cells [4]. CLV3 encodes the presumed ligand for a heteromeric complex comprising the Clv2 and Clv1 proteins, which accumulate in the more interior L3 layer. The active Clavata complex then negatively regulates WUS expression by an unknown mechanism. WUS, which encodes a homeodomain-type transcription factor, in turn is a positive regulator of CLV3 expression. The mechanism by which CLV3 expression is activated is still unknown, as WUS is expressed in different cells than CLV3. This negative feedback loop insures that stem cells are restricted to the centre of the SAM and its distribution across all three layers ensures coordinated regulation of stem cell numbers throughout the central zone. Classical analysis of mutant phenotypes has played a key role in ascribing specific function to individual genes within this interacting network. Plants defective in CLV3 have enlarged meristems, caused by a large expansion of the central zone (Figure 1). Several mechanisms have been proposed to explain this: increased proliferation in the central zone, re-specification of peripheral cells to central cells or decreased ability of cells at the periphery to organize into organ primordia [5–7]. From the finding of low cell division rates throughout the enlarged SAM …