Epigenetic Regulation of Gene Programs by EMF1 and EMF2 in Arabidopsis    

Abstract

The EMBRYONIC FLOWER (EMF) genes are required to maintain vegetative development in Arabidopsis (Arabidopsis thaliana). Loss-of-function emf mutants skip the vegetative phase, flower upon germination, and display pleiotropic phenotypes. EMF1 encodes a putative transcriptional regulator, while EMF2 encodes a Polycomb group (PcG) protein. PcG proteins form protein complexes that maintain gene silencing via histone modification. They are known to function as master regulators repressing multiple gene programs. Both EMF1 and EMF2 participate in PcG-mediated silencing of the flower homeotic genes AGAMOUS, PISTILLATA, and APETALA3. Full-genome expression pattern analysis of emf mutants showed that both EMF proteins regulate additional gene programs, including photosynthesis, seed development, hormone, stress, and cold signaling. Chromatin immunoprecipitation was carried out to investigate whether EMF regulates these genes directly. It was determined that EMF1 and EMF2 interact with genes encoding the transcription factors ABSCISIC ACID INSENSITIVE3, LONG VEGETATIVE PHASE1, and FLOWERING LOCUS C, which control seed development, stress and cold signaling, and flowering, respectively. Our results suggest that the two EMFs repress the regulatory genes of individual gene programs to effectively silence the genetic pathways necessary for vegetative development and stress response. A model of the regulatory network mediated by EMF is proposed.

Deciphering the Role of POLYCOMB REPRESSIVE COMPLEX1 Variants in Regulating the Acquisition of Flowering Competence in Arabidopsis

“…On the other hand, other results suggest that all these components are required for the regulation of a different subset of target genes. For instance, AtRING1A has been shown to participate in the repression of FLC, MAF4, and MAF5 (Shen et al, 2014) and EMF1 in the repression of FLC (Kim et al, 2010). We show here that both EMF1 and AtBMI1 are required for FLC, MAF4, and MAF5 repression, suggesting a PRC1 in which AtRING1, AtBMI1, and EMF1 are required for repression.…”

“…As CO transcription is low at ZT1 and its expression is not altered in emf1 and emf2 mutants (Kim et al, 2010), the FT misexpression in these mutants may be CO independent. In support of this, it has been shown that emf1-1/co and emf2/co double mutant phenotypes were indistinguishable from their respective emf1 and emf2 single mutant parents, while emf1-1/ft double mutants usually did not flower and emf2/ft double mutants bolted after producing a higher number of sessile leaves than emf2 single mutants (Haung and Yang, 1998).…”

EMBRYONIC FLOWER1 and ULTRAPETALA1 Act Antagonistically on Arabidopsis Development and Stress Response

“…To understand the function of the LFYasEMF1 misregulated genes restored by ult1-3, we considered the 15 functional categories described previously (Kim et al, 2010), with appropriate modifications of the gene list. These categories include genes involved in flower organ identity, flowering time, seed development, photoreceptor and photosynthesis system, cell expansion, auxin, GA, ethylene, and abscisic acid synthesis and signaling, stress, cold, and heat responses, and histone and transcription factor genes (Supplemental Table S1).…”

“…Mutations in EMF1 and EMF2 cause plants to skip the vegetative phase, transforming the embryonic meristem from an indeterminate to a determinate state and producing a terminal flower (Sung et al, 1992;Yang et al, 1995;Chen et al, 1997;Yoshida et al, 2001). Global gene expression analysis revealed that EMF1 regulates a remarkably high number of genes involved in transcription factor activity, developmental pathways, microRNA gene silencing, and stress responses in Arabidopsis (Kim et al, 2010). Tissue-specific removal of EMF1 activity from leaf primordia in transgenic plants expressing antisenseEMF1 under the control of the LEAFY (LFY) promoter (LFYasEMF1) permits vegetative growth but leads to early flowering plants with upward-curled leaves (Sánchez et al, 2009) similar to those of curly leaf (clf), a PcG mutant (Goodrich et al, 1997).…”

“…Although EMF1 shares no sequence homology with animal PcG protein genes, it is involved in plant PcG-mediated gene repression and targets flower homeotic genes directly, as does EMF2 (Kim et al, 2010). Mutations in EMF1 and EMF2 cause plants to skip the vegetative phase, transforming the embryonic meristem from an indeterminate to a determinate state and producing a terminal flower (Sung et al, 1992;Yang et al, 1995;Chen et al, 1997;Yoshida et al, 2001).…”