Antagonistic Roles of SEPALLATA3, FT and FLC Genes as Targets of the Polycomb Group Gene CURLY LEAF

Manuel Lopez-Vernaza,Ralf Müller,Frazer Thorpe,Suxin Yang,Justin Goodrich,Erica De Leau

doi:10.1371/journal.pone.0030715

Abstract

In Arabidopsis, mutations in the Pc-G gene CURLY LEAF (CLF) give early flowering plants with curled leaves. This phenotype is caused by mis-expression of the floral homeotic gene AGAMOUS (AG) in leaves, so that ag mutations largely suppress the clf phenotype. Here, we identify three mutations that suppress clf despite maintaining high AG expression. We show that the suppressors correspond to mutations in FPA and FT, two genes promoting flowering, and in SEPALLATA3 (SEP3) which encodes a co-factor for AG protein. The suppression of the clf phenotype is correlated with low SEP3 expression in all case and reveals that SEP3 has a role in promoting flowering in addition to its role in controlling floral organ identity. Genetic analysis of clf ft mutants indicates that CLF promotes flowering by reducing expression of FLC, a repressor of flowering. We conclude that SEP3 is the key target mediating the clf phenotype, and that the antagonistic effects of CLF target genes masks a role for CLF in promoting flowering.

Highlights

Plants usually flower at specific times of year, in order to align flowering with periods when pollinators are available and conditions are favourable for growth and fruit set
Because there is considerable redundancy between the closely related Pc-G genes CURLY LEAF (CLF) and SWN [23] even null clf mutants have an intermediate level of Pc-G activity; we reasoned that the clf phenotype would be sensitised to small changes in activity of CLF target genes, for example due to mutations in the target genes themselves or in genes that regulate their activity such as trx-G or Pc-G members
Previous work showed that AG is necessary for the clf phenotype and that mis-expression of AG causes leaf curling [3,46]

Summary

Introduction

Plants usually flower at specific times of year, in order to align flowering with periods when pollinators are available and conditions are favourable for growth and fruit set. To achieve this, flowering time is regulated by environmental signals, primarily temperature and photoperiod, and by intrinsic factors such as the age of a plant. Genetic analysis in Arabidopsis has identified the key components of several flowering pathways, including the photoperiod and vernalization pathways, which mediate responses to daylength and temperature, and the autonomous pathway, which promotes flowering independently of environmental signals [1]. Genetic analysis suggests that flowering is controlled epigenetically, through factors that act on chromatin of these integrator genes to alter their transcriptional activity. The epigenetic control of flowering is best defined for the vernalization pathway, where long periods of cold such as occur in winter trigger a stable epigenetic change that promotes flowering [2]. The Pc-G regulate genes with opposite effects on flowering, and the relevance of this has not been clear [5]

Methods

Results

Conclusion