Polycomb Group (PcG) proteins are responsible for post-transcriptional modifications in histone tails leading to chromatin condensation and changes in gene expression. In Arabidopsis thaliana, curly leaf (CLF) is a member of the Polycomb Reporssive Complex 2 (PRC2), which cnfers a repressive epigenetic mark, namely trimethylation of histone H3 at lysine 27 (H3K27me3). In the clf mutant, the expression of the floral organ identity gene AGAMOUS (AG) is derepressed in vegetative stages and coincides with loss of H3K27me3 at the AG locus. Recent whole genome prfiling studies have suggested that PcG genes regulate mang more developmental regulators than AG (about 15% of Arabidopis genes). However, it remains unclear what the relevance of PcG regulation of these targets is for plant development; in addition, it is not known how changes in J3K27me3 casue gene repression in plants. To unravel the role of CLFcin A. thaliana, a T-DNA mutagenesis in the clf background was performed to identify mutations enhancing or suppressing the Clf- phenotype, as these may identify additional PcG genes and targets. Firstly, I screened an A. thaliana T-DNA mutagenized population and identified four mutations suppressing the Clf- phenotype: suppressor of polycomb 1 to 4 (sop1, sop2, sop3 and sop4). Secondly, I characterized these four mutants. The sop1 mutant had normal flowering time and the suppressed phenotype is due to a loss of function mutation in SEPALLATA3 (SEP3). I establied the SEP3 is an activator and a co-factor of AG. Also, I found that SEP3 is stronlgy mis-expressed in clf mutants and SEP3 chromatin is enriched the H3K27me3, which stronly suggests that SEP3 is a direct target of CLF. In addition, I showed that a mutation in Flowering Locus T (FT), which is a positive regulator of SEP3, suppreesed the Clf- phenotype suggesting the FT is also a target of CLF. Suppressors sop3, sop3 and sop4 are late flowering, unlike sop1, and show increased expression of Flowering Locus C (FLC), a MADS-box transcription factor gene that represses flowering. I found that the sop4 mutation in likely casued by disruption of FPA, a predicted RNA binding protein that promotes flowering time by repressing FLC. Consistent with this, sop4 mutants show hight levels of FLC. Unexpectedly, fpa clf (sop4) mutatns are much later flowering than clf FRI mutants, which have similarly high levels of FLC. This suggests that FPA may regulate other genes controlling flowering thant FLC. The genes involved in sop2 and sop3 mutants remain to be identified. In this thesis I brought genetic and molecular evidence showing that CLF, though the PRC2, control floral induction (FLC), floral integration (FT) and floral organ formation (SEP3 and AG) in A. thaliana.