Floral organs, whose identity is determined by specific combinations of homeotic genes, originate from a group of undifferentiated cells called the floral meristem. In Arabidopsis, the homeotic gene AGAMOUS(AG) terminates meristem activity and promotes development of stamens and carpels. To understand the program of gene expression activated by AG, we followed genome-wide expression during early stamen and carpel development. The AG target genes included most genes for which mutant screens revealed a function downstream of AG. Novel targets were validated by in situ hybridisation and binding to AG in vitro and in vivo. Transcription factors formed a large fraction of AG targets, suggesting that during early organogenesis, much of the genetic program is concerned with elaborating gene expression patterns. The results also suggest that AG and other homeotic proteins with which it interacts (SEPALLATA3, APETALA3,PISTILLATA) are coordinately regulated in a positive-feedback loop to maintain their own expression, and that AG activates biosynthesis of gibberellin, which has been proposed to promote the shift from meristem identity to differentiation.

We have characterized Arabidopsis esd1 mutations, which cause early flowering independently of photoperiod, moderate increase of hypocotyl length, shortened inflorescence internodes, and altered leaf and flower development. Phenotypic analyses of double mutants with mutations at different loci of the flowering inductive pathways suggest that esd1 abolishes the FLC-mediated late flowering phenotype of plants carrying active alleles of FRI and of mutants of the autonomous pathway. We found that ESD1 is required for the expression of the FLC repressor to levels that inhibit flowering. However, the effect of esd1 in a flc-3 null genetic background and the downregulation of other members of the FLC-like/MAF gene family in esd1 mutants suggest that flowering inhibition mediated by ESD1 occurs through both FLC-and FLC-like gene-dependent pathways. The ESD1 locus was identified through a map-based cloning approach. ESD1 encodes ARP6, a homolog of the actin-related protein family that shares moderate sequence homology with conventional actins. Using chromatin immunoprecipitation (ChIP) experiments, we have determined that ARP6 is required for both histone acetylation and methylation of the FLC chromatin in Arabidopsis. Development 133, 1241Development 133, -1252Development 133, (2006 DEVELOPMENT 1242 and the trimethylation of lysine 4 of H3 (H3-K4), which are hallmarks of active genes (He et al., 2003; Ausin et al., 2004; He et al., 2004). Late-flowering autonomous pathway mutants also have increased levels of H3-K4 trimethylation and histone acetylation compared with the rapid-flowering parental line (He et al., 2003; Ausin et al., 2004; He et al., 2004;Kim et al., 2005). Many early flowering mutations suppressing the late flowering phenotype of FRI-containing lines have identified components that are required to maintain high levels of FLC expression. This is the case of mutants such as early flowering in short days (efs), photoperiod independent early flowering 1 (pie1), early flowering 5 (elf5), vernalization independence3 (vip3) and frigida-like1 (frl-1), and mutants in genes encoding components of the PAF1 complex (ELF7, VIP4, VIP5 and VIP6/ELF8) (Zhang and Van Nocker, 2002;Noh and Amasino, 2003;Zhang et al., 2003;Noh et al., 2004; He et al., 2004;Michaels et al., 2004;Oh et al., 2004;Kim et al., 2005). Most of these mutations also appear to affect flowering in an FLC-independent manner. KEY WORDS: Flowering time, Floral repression, Chromatin remodelling, ArabidopsisAfter exposure to an extended winter and the completion of vernalization, the level of modifications associated with 'active' chromatin is reduced, and the histone tails of FLC chromatin are deacetylated and become enriched in methylation of lysine 9 (K9) and 27 (K27) of H3 (Bastow et al., 2004;Sung and Amasino, 2004), which are hallmarks of repressed genes (Orlando, 2003). Mutants that are unable to reduce FLC transcript levels by vernalization or to maintain the vernalised state have permitted the identification of some of the proteins particip...

SummaryConditions to promote dark morphogenesis and¯ower-ing in Arabidopsis have previously been limited to liquid cultures and to a few laboratory ecotypes. We have obtained development and¯owering of Arabidopsis plants under complete darkness by growing them on vertical Petri dishes containing solid agar medium with sucrose. Under these conditions, all the ecotypes tested were able to develop, giving rise to etiolated plants that¯owered after producing a certain number of leaves. Dark-grown plants showed similarities with phytochrome-de®cient mutants and were different from de-etiolated or constitutive photomorphogenesis mutants such as det and cop. Late-and early-¯owering ecotypes, showing large differences in¯owering time and leaf number under long days,¯owered with a similar number of leaves when grown in the dark. Rapid dark¯owering of late-¯owering ecotypes was not an effect of darkness but the result of the interaction between dark and sucrose availability at the aerial part of the plant, since sucrose also had an effect when plants were grown in the light. Gibberellin-de®cient and insensitive mutants were delayed in the initiation of owers in the dark, indicating a role for these hormones in¯owering promotion in the dark. The late-¯owering phenotype of mutants at different loci of the autonomous and long-day-dependent¯owering induction pathways was rescued in dark growth conditions. However, the late-¯owering phenotype of ft and fwa mutants was not rescued by sucrose either in the dark or in the light, suggesting a different role for these genes in¯owering induction.