EARLY IN SHORT DAYS 1(ESD1) encodes ACTIN-RELATED PROTEIN 6 (AtARP6), a putative component of chromatin remodelling complexes that positively regulatesFLCaccumulation inArabidopsis

Abstract

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...

The FRIGIDA Complex Activates Transcription of FLC, a Strong Flowering Repressor in Arabidopsis, by Recruiting Chromatin Modification Factors

“…By contrast, the mutations cause the suppression of the developmentally regulated FLC gene, supporting the positive role of H2A. Z (Martin-Trillo et al, 2006;Choi et al, 2007;Deal et al, 2007;March-Díaz et al, 2007).…”

The BAF60 Subunit of the SWI/SNF Chromatin-Remodeling Complex Directly Controls the Formation of a Gene Loop at FLOWERING LOCUS C in Arabidopsis

“…This complex is involved in the substitution of histone H2A by the histone variant H2A.Z (March-Díaz and Reyes, 2009). Indeed, mutations in PIE1, ARP6 (also known as SUF3 and ESD1 in Arabidopsis), and SEF/ AtSW6C show early flowering and reduced FLC expression (Noh and Amasino, 2003;Choi et al, 2005Choi et al, , 2007Deal et al, 2005;Martin-Trillo et al, 2006;March-Díaz et al, 2007;Lázaro et al, 2008), and ARP6 and PIE1 were found to be required for H2A.Z deposition at FLC (Deal et al, 2007). Finally, it has been shown that disruption of BRM results in high FLC expression and that the brm mutation restores high accumulation of FLC mRNA in pie and sef mutants, suggesting that SWR1/SCRAP and SWI/SNF complexes play antagonistic roles in FLC regulation (Farrona et al, 2011).…”

Repression of Flowering inArabidopsisRequires Activation ofFLOWERING LOCUS CExpression by the Histone Variant H2A.Z

“…Previous work in Arabidopsis showed that loss-of-function mutations in two genes encoding putative homologs of components of the SWR1/SRCAP complex, ACTIN-RELATED PROTEIN6 (ARP6) and the Snf2 protein PHOTOPERIOD-INDEPENDENT EARLY FLOWERING1 (PIE1), led to premature flowering as a result of reduced FLC expression (Noh and Amasino, 2003;Choi et al, 2005;Deal et al, 2005;Martin-Trillo et al, 2006). However, the mechanism by which these proteins regulate FLC expression has not been addressed.…”