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Plant longevity depends on reservoirs of slowly proliferating stem cells, where a reduced rate of division is essential for maintaining DNA integrity. Aboveground stem cells are localized in the central zone of the shoot meristems, whose size is controlled by the transcription factor WUS. This review focuses on the mechanism of WUS function and the regulation of its expression. WUS maintains the central zone's size by controlling the hormones such as cytokinins. It forms complexes with various transcription factors and can act as a repressor and an activator of gene transcription. Cytokinins define WUS spatial expression relative to the meristem surface, while EPFL signaling limits WUS radial expansion. CLV3 signaling modulates WUS expression levels within the boundaries set by cytokinin and EPFLs. A significant overlap of WUS and CLV3 expression in the L3 layer suggests that autocrine signaling by CLV3 may play a central role in regulating WUS expression. 

ABSTRACT The shoot apical meristem (SAM) gives rise to the aboveground organs of plants. The size of the SAM is relatively constant due to the balance between stem cell replenishment and cell recruitment into new organs. In angiosperms, the transcription factor WUSCHEL (WUS) promotes stem cell proliferation in the central zone of the SAM. WUS forms a negative feedback loop with a signaling pathway activated by CLAVATA3 (CLV3). In the periphery of the SAM, the ERECTA family receptors (ERfs) constrain WUS and CLV3 expression. Here, we show that four ligands of ERfs redundantly inhibit the expression of these two genes. Transcriptome analysis confirmed that WUS and CLV3 are the main targets of ERf signaling and uncovered new ones. Analysis of promoter reporters indicated that the WUS expression domain mostly overlaps with the CLV3 domain and does not shift along the apical-basal axis in clv3 mutants. Our three-dimensional mathematical model captured gene expression distributions at the single-cell level under various perturbed conditions. Based on our findings, CLV3 regulates cellular levels of WUS mostly through autocrine signaling, and ERfs regulate the spatial expression of WUS, preventing its encroachment into the peripheral zone.