Vernalization is the acquisition of floral competence through exposure to prolonged cold in winter. In Arabidopsis, the two strong floral repressors FRIGIDA (FRI) and FLOWERING

INTRODUCTION During eukaryotic chromosome replication, both genetic and epigenetic information are accurately duplicated, which maintains identical cellular memory through mitoses (Margueron and Reinberg, 2010). DNA replication accompanies chromatin assembly, and the cooperation between these two processes has long been proposed to be important for the mitotic maintenance of epigenetic information (Alabert and Groth, 2012; Ransom et al., 2010; Smith and Whitehouse, 2012). DNA polymerase α is responsible for initiating replication at both the origins and the lagging strand (Kunkel and Burgers, 2008). In Arabidopsis, the single copy gene INCURVATA2 (ICU2) encodes the catalytic subunit of DNA polymerase α, and transfer DNA (T-DNA)-inserted knockout mutants of ICU2 showed a lethal phenotype during gametogenesis and embryogenesis (Barrero et al., 2007). A missense mutation in ICU2, icu2-1, was isolated by the resulting upward curling phenotype of the rosette leaves (Serrano-Cartagena et al., 2000). This mutant exhibits early flowering and homeotic transition of the floral organs, as observed in mutants of Polycomb Repressive Complex 2 (PRC2) (Barrero et al., 2007). Accordingly, certain PRC2 target genes are de-regulated in icu2-1 (Barrero et al., 2007). Another missense allele of ICU2, polα, was identified by suppressor mutant screening of the repressor of transcriptional silencing 1 (ros1) (Liu et al., 2010a), which has a defect in the DNA demethylase ROS1 (Gong et al., 2002). The polα mutant exhibited a similar phenotype to icu2-1, and showed de-repression of some heterochromatic elements in the Arabidopsis genome, although the DNA methylation levels in the centromeric repeats and transposons were not affected. ICU2 has a genetic relationship with CURLY LEAF (CLF), a SET-domain component of PRC2; LIKE-HETEROCHROMATIN PROTEIN 1 (LHP1), a potential PRC1 component; and FASCIATA1 (FAS1), a chromatin assembly factor (Barrero et al., 2007). The vernalization response in Arabidopsis thaliana is an example of the mitotic inheritance of histone marks in plants (Kim et al., 2009). Vernalization is the acquisition of floral competence through exposure to prolonged cold in winter. In Arabidopsis, the two strong floral repressors FRIGIDA (FRI) and FLOWERING LOCUS C (FLC) synergistically interact to cause late flowering (Shindo et al., 2005). FRI induces the expression of FLC, and the resulting high level of FLC inhibits floral induction. However, vernalization induces the downregulation of FLC, and this repression is mitotically remembered until reproduction, even after a return to warm conditions (Choi et al., 2009; Kim et al., 2009; Sheldon et al., 2008). As a result, plants exposed to long-term cold treatment undergo the transition to flowering. Covalent histone modifications at the FLC genomic region is a key process for maintaining FLC repression (Kim et al., 2009). During vernalization, FLC repression is initiated by VERNALIZATION INSENSITIVE 3 (VIN3) through the deacetylation of histone H3. Simultaneously, VERNALIZATION2 (VRN2)-PRC2 deposits H3K27me3 at the FLC region (De Lucia et al., 2008; Finnegan and Dennis, 2007; Sung and Amasino, 2004; Wood et al., 2006). The accumulation of H3K27me3 results in the stable repression of FLC. Accordingly, a loss-of-function vrn2 mutant normally shows a downregulation of FLC during vernalization. However, the mutant fails to accumulate H3K27me3, so FLC is de-repressed when the vrn2 plants return to warm conditions (Gendall et al., 2001). Remarkably, the H3K27me3 mark is inherited and propagated to nearby histones in the FLC 1Department of Biological Sciences, Seoul National University, Seoul, 151-742, Korea. 2Section of Molecular Cell and Developmental Biology and Institute for Cellular and Molecular Biology, University of Texas at Austin, TX 78712, USA. 3Plant Genomics and Breeding Institute, Seoul National University, Seoul 151-747, Korea.