No abstract

The Arabidopsis thaliana early in short days6 (esd6) mutant was isolated in a screen for mutations that accelerate flowering time. Among other developmental alterations, esd6 displays early flowering in both long-and short-day conditions. Fine mapping of the mutation showed that the esd6 phenotype is caused by a lesion in the HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENES1 (HOS1) locus, which encodes a RING finger-containing E3 ubiquitin ligase. The esd6/hos1 mutation causes decreased FLOWERING LOCUS C expression and requires CONSTANS (CO) protein for its early flowering phenotype under long days. Moreover, CO and HOS1 physically interact in vitro and in planta, and HOS1 regulates CO abundance, particularly during the daylight period. Accordingly, hos1 causes a shift in the regular long-day pattern of expression of FLOWERING LOCUS T (FT ) transcript, starting to rise 4 h after dawn in the mutant. In addition, HOS1 interacts synergistically with CONSTITUTIVE PHOTOMORPHOGENIC1, another regulator of CO protein stability, in the regulation of flowering time. Taken together, these results indicate that HOS1 is involved in the control of CO abundance, ensuring that CO activation of FT occurs only when the light period reaches a certain length and preventing precocious flowering in Arabidopsis.

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...