Local accumulation of the plant growth regulator auxin mediates pattern formation in Arabidopsis roots and influences outgrowth and development of lateral root- and shoot-derived primordia. However, it has remained unclear how auxin can simultaneously regulate patterning and organ outgrowth and how its distribution is stabilized in a primordium-specific manner. Here we show that five PIN genes collectively control auxin distribution to regulate cell division and cell expansion in the primary root. Furthermore, the joint action of these genes has an important role in pattern formation by focusing the auxin maximum and restricting the expression domain of PLETHORA (PLT) genes, major determinants for root stem cell specification. In turn, PLT genes are required for PIN gene transcription to stabilize the auxin maximum at the distal root tip. Our data reveal an interaction network of auxin transport facilitators and root fate determinants that control patterning and growth of the root primordium.

Stem cells self-renew and produce daughter cells that differentiate. How stem cells are specified and maintained is a central question in developmental biology. Plant stem cells occupy a small region or niche in larger zones of mitotic activity called meristems. Here we provide molecular evidence that in the Arabidopsis root meristem, the stem cell population depends on a central group of cells, the quiescent center (QC), which positions the stem cell niche. We show that the putative transcription factor SCARECROW (SCR), first identified by its role in radial patterning, is required cell-autonomously for distal specification of the QC, which in turn regulates stem cell fate of immediately surrounding cells. Received October 21, 2002; revised version accepted November 29, 2002. Stem cell identity in various organisms is maintained in microenvironments called niches (Spradling et al. 2000). Their maintenance depends on local signaling events emanating from nearby cells that can be considered part of the niche (Spradling et al. 2000). Cap cells (Xie and Spradling 1998, 2000) and somatic hub cells (Kiger et al. 2001;Tulina and Matunis 2001) in Drosophila, distal tip cells in Caenorhabditis elegans (Kimble and White 1981), and cells expressing the homeodomain transcription factor WUSCHEL in the Arabidopsis shoot apical meristem (Mayer et al. 1998;Schoof et al. 2000) are examples of cells locally required for the maintenance of stem cells. In these cases, it remains to be established how the signaling cells themselves are specified to define stem cell location.In the Arabidopsis root meristem, the "initial cells" are the stem cells that give rise to all cell types of the root; they surround a small group of mitotically less active cells, the quiescent center (QC), and can be unequivocally identified (Fig. 1a;Dolan et al. 1993). Laser ablation experiments suggested that the QC is a source of cell nonautonomous signals, which prevent differentiation and hence maintain the surrounding stem cells (van den Berg et al. 1997). Hence, the QC and the surrounding cells that contact it can be considered a stem cell niche. The SCARECROW (SCR) gene encodes a putative transcription factor (Di Laurenzio et al. 1996) that is first expressed in QC precursor cells during embryogenesis, after which it extends to the initial cells for the ground tissue (cortex and endodermis) and the endodermis ; this expression pattern persists in the postembryonic root ( Fig. 1a; Di Laurenzio et al. 1996). In scr-1 mutants, the asymmetric cell division of the daughter of the cortex/endodermis initial does not occur, resulting in a single cell layer with mixed identity ( Fig. 1d; Di Laurenzio et al. 1996). Importantly, cells in the src-1 QC region are aberrant in shape and roots ultimately cease growth (Scheres et al. 1995;Di Laurenzio et al. 1996). Here, we provide evidence that these effects are not caused by the cortex/endodermis defect but rather reflect a direct requirement for SCR activity in QC cells for their specification and maintenance ...

The maintenance of stem cells in defined locations is crucial for all multicellular organisms. Although intrinsic factors and signals for stem cell fate have been identified in several species, it has remained unclear how these connect to the ability to reenter the cell cycle that is one of the defining properties of stem cells. We show that local reduction of expression of the RETINOBLASTOMA-RELATED (RBR) gene in Arabidopsis roots increases the amount of stem cells without affecting cell cycle duration in mitotically active cells. Conversely, induced RBR overexpression dissipates stem cells prior to arresting other mitotic cells. Overexpression of D cyclins, KIP-related proteins, and E2F factors also affects root stem cell pool size, and genetic interactions suggest that these factors function in a canonical RBR pathway to regulate somatic stem cells. Expression analysis and genetic interactions position RBR-mediated regulation of the stem cell state downstream of the patterning gene SCARECROW.

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Tissue-specific stem cells combine proliferative and asymmetric divisions to balance self-renewal with differentiation. Tight regulation of the orientation and plane of cell division is crucial in this process. Here, we study the reproducible pattern of anterior-posterior-oriented stem cell-like divisions in the Caenorhabditis elegans seam epithelium. In a genetic screen, we identified an alg-1 Argonaute mutant with additional and abnormally oriented seam cell divisions. ALG-1 is the main subunit of the microRNA-induced silencing complex (miRISC) and was previously shown to regulate the timing of postembryonic development. Time-lapse fluorescence microscopy of developing larvae revealed that reduced alg-1 function successively interferes with Wnt signaling, cell adhesion, cell shape and the orientation and timing of seam cell division. We found that Wnt inactivation, through mig-14 Wntless mutation, disrupts tissue polarity but not anterior-posterior division. However, combined Wnt inhibition and cell shape alteration resulted in disordered orientation of seam cell division, similar to the alg-1 mutant. Our findings reveal additional alg-1-regulated processes, uncover a previously unknown function of Wnt ligands in seam tissue polarity, and show that Wnt signaling and geometric cues redundantly control the seam cell division axis.