SeeDev-binary@ldeleger:SeeDev-binary-16387832-2 / 2300-2303
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Postembryonic organ formation in plants requires the maintenance of small stem cell pools in the shoot, floral, and root meristems
(Weigel and Jürgens, 2002; Laux, 2003). Similar to animal stem cell systems, the meristems provide a microenvironment, the stem cell niche, in which differentiation
of the resident cells is repressed, whereas daughter cells that leave this site undergo differentiation. In the Arabidopsis thaliana shoot meristem, the stem cells are located in the three outermost cell layers of the most central region of the shoot apex.
The stem cells cannot be distinguished by their appearance from the surrounding meristem cells, and stem cell function can
only be unambiguously identified by clonal studies (Stewart and Dermen, 1970). Expression of CLAVATA3 (CLV3) mRNA (Fletcher et al., 1999) that coincides with the presumed position of the apical stem cells provides an operational marker for stem cell identity
in the shoot meristem.
Only a few mutants have been isolated that specifically fail to protect shoot meristem stem cells from differentiation. One
of the genes identified from mutant studies encodes the homeodomain protein WUSCHEL (WUS). WUS is expressed in a domain underneath the stem cells termed the organizing center (OC) and is required and sufficient to maintain
the overlying stem cells undifferentiated (Mayer et al., 1998; Schoof et al., 2000). The stem cells in turn signal back via the CLV3 peptide to restrict the size of the OC, thereby creating a negative feedback
loop to dynamically control the size of the stem cell population (Brand et al., 2000; Schoof et al., 2000). CLV3 presumably acts as an extracellular ligand of the CLV1 receptor kinase complex, which eventually leads to downregulation
of WUS transcription in the recipient cells (Clark et al., 1997; Stone et al., 1998; Trotochaud et al., 1999; Rojo et al., 2002; Lenhard and Laux, 2003). In floral meristems that are homologous to indeterminate shoot meristems, the AGAMOUS (AG) gene represses WUS expression late in flower development to terminate the stem cell niche after a limited number of organs have been formed
(Lenhard et al., 2001; Lohmann et al., 2001).
The primary shoot meristem is formed during embryo development (Barton and Poethig, 1993). In Arabidopsis, the onset of WUS expression in precursor cells of the OC in the 16-cell embryo suggests that shoot meristem formation has been initiated already
at this stage (Mayer et al., 1998). CLV3 expression is detected from late heart stage on between the outgrowing cotyledons (Fletcher et al., 1999). In bent cotyledon embryos, the primary shoot meristem becomes visible as a bulge of small cytoplasmic cells that after
germination give rise to a rosette of leaves before an inflorescence stem is formed, carrying cauline leaves with axillary
shoot meristems and bractless floral meristems.
Many aspects of the mechanisms that operate in the stem cell niches to maintain stem cells undifferentiated are not understood
and might have escaped genetic analysis due to genetic redundancy. Therefore, we performed an extensive genetic screen to
detect presumably rare dominant-negative mutations affecting stem cell maintenance. Here, we report the isolation and functional
characterization of the semidominant l28 mutant that in the homozygous state is unable to keep stem cells undifferentiated similar to the wus mutant. We show that the premature termination of the shoot meristem in l28 mutants is caused by a mutation in the APETALA2 (AP2) gene that was previously identified as one of the components of the ABC model in floral patterning, where it represses AG (Bowman et al., 1991; Drews et al., 1991), in floral transition (Jofuku et al., 1994; Okamuro et al., 1997b), and in the control of seed size (Jofuku et al., 2005; Ohto et al., 2005).
In this article, we show that maintenance of the stem cell niche in the primary shoot meristem requires the activity of AP2 and redundant factor(s) via an AG independent mechanism that involves interaction with the WUS-CLV3 feedback loop.
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