Transcription repressor that regulates phase transition during shoot, flower and seeds development. Controls leaves development, shoot architecture and flowering by delaying both the vegetative to reproductive transition and flower initiation. Participates in polycomb group (PcG) protein complex-mediated (including EMF2) silencing of the flower homeotic genes AGAMOUS (AG), PISTILLATA (PI), and APETALA3 (AP3), as well as of some regulatory genes such as ABSCISIC ACID INSENSITIVE3 (ABI3), LONG VEGETATIVE PHASE1 (LOV1), and FLOWERING LOCUS C (FLC) during vegetative development. Required for histone methylation or for maintaining a stable histone methylation (e.g. H3K27me3) pattern of repressed target genes (including genes involved in salt stress response and flower development); this repression is counteracted by ULT1 (PubMed:23632855). Can bind non specifically DNA (both double- and single-stranded) and RNA. Interacts with MSI1. Follow a speckle-like pattern. Expressed in mature embryo, root tips, cotyledons, leaves, stems, shoot apex, and flower clusters, with highest levels in flowers. The presence in the shoot apical meristem (SAM) is required to maintain vegetative development and prevent early flowering. After flowering, expressed in the stigma and anthers. Abolished rosette shoot development, reduced inflorescence with several flowers lacking petals, and differentiation of the apical meristem from indeterminate to determinate growth by producing a single terminal flower on all nodes. Altered inflorescence-to-flower transition. Degenerated flowers with only carpelloid structures capped with stigmatic papillae but lacking leaves, petals and stamen. Derepressed seed development program. Decreased H3K27me3 marks but increased H3K4me3 marks on target gene loci (PubMed:23632855). Plants missing both EMF1 and ULT1 have rescued normal H3K27me3 marks and H3K4me3 marks (PubMed:23632855).