Study on the Role of EARLY FLOWERING AND CURLY LEAVES (EFC) in the FIS2-PRC2 Complex of Arabidopsis thaliana

Abstract

The Polycomb Repressive Complex 2 (PRC2) is known as one of the master epigenetic regulators in both plants and mammals. It represses transcriptional activity of genes that are not required at specific formative stages by trimethylation of lysine 27 on histone H3 (H3K27me3). In a previous study, a gain-of-function mutant, early flowering and curly leaves-D (efc-D) was isolated from a population of activation tagging mutants. Overexpression of EFC caused increased expression levels of PRC2 target genes, such as FLOWERING LOCUS C (FLC), FLOWERING LOCUS T (FT) and AGAMOUS (AG). Among three PRC2 complexes in Arabidopsis thaliana, the FERTILIZATION INDEPENDENT SEED2-PRC2 complex plays essential roles in endosperm development by regulating genes in the central cell and endosperm. Interestingly, EFC was specifically expressed in nuclei of the central cell and endosperm and interacted with MSI1, one of the core members of the PRC2. In this study I characterized a loss-of-function mutant efc-1. The efc-1 mutation caused a seed abortion in Arabidopsis. EFC showed a partial or incomplete penetrance. The expression of MEDEA (MEA) and UPWARD CURLY LEAF1 (UCL1), genes that are regulated by FIS2-PRC2, were derepressed in the central cell or endosperm of the efc-1 mutant. I carried out a complementation experiment of fis2 with EMBRYONIC FLOWER2 (EMF2), a homolog of FIS2, in the seed in absence of EFC. Presumably due to the partial penetrance of EFC, there was no significant complementation observed in the heterozygous efc-1

heterozygous fis2-11 and hemizygous FIS2::EMF2 triple mutant plants. Therefore, it needs to be checked in the next generation when I obtain a triple homozygous mutant or double homozygous and fis2-11 heterozygous mutant. The results so far may suggest that EFC might play a role in seed development along with the FIS2-PRC2 complex, however not essential.