SeeDev-binary@ldeleger:SeeDev-binary-16387832-3 JSONTXT

Continuous organ formation from the shoot meristem during the postembryonic life of higher plants depends on the maintenance of undifferentiated stem cells in specific microenvironments, named stem cell niches (Weigel and Jürgens, 2002; Laux, 2003). Here, we identify a novel regulatory pathway in shoot meristem stem cell maintenance defined by AP2 function. Stem Cell Maintenance Is Regulated by AP2AP2 was originally identified as a floral homeotic gene encoding A-function of the ABC model of organ identity specification (Bowman et al., 1989, 1991). Recently, it has also been implicated in floral transition and control of seed size (Okamuro et al., 1997b; Jofuku et al., 2005; Ohto et al., 2005). Here, we show that l28 and l28/+ plants have a number of phenotypes in common with ap2 loss-of-function alleles, such as early flowering, mispecified floral organs, and a reduction in shoot meristem size. By contrast, premature termination of the shoot meristem and differentiation of the stem cells is only observed in the l28 allele. Wild-type AP2 is expressed in the shoot meristem at all stages, consistent with an as yet unknown function there. Our gene dosage experiments indicate that wild-type AP2 activity competes with l28 activity. A plausible interpretation of these data is that l28 acts as a dominant-negative allele of AP2 and thus identifies a novel pathway in shoot meristem development. Definite proof of this model has to await the identification of potential redundant factors that appear to mask AP2 function in the shoot meristem. The l28 mutation changes a highly conserved negatively charged Glu residue into a positively charged Lys residue within the first of the two putative DNA binding domains of AP2. A possible model is therefore that the mutant protein competes with wild-type AP2 and redundant factor(s) for interactors in a protein complex but compromises its binding to DNA targets. Alternatively, the mutant protein may still be able to bind to AP2 target genes but fail to interact with cofactors required for transcriptional regulation. Stochastic variations in the balance between mutant and redundant wild-type proteins might account for the differences when meristem termination occurs in individual homozygous l28 mutants.