The Arabidopsis Paf1c complex component CDC73 participates in the modification of FLOWERING LOCUS C chromatin.

Abstract:

:FLOWERING LOCUS C (FLC) is a key repressor of flowering in Arabidopsis (Arabidopsis thaliana) and is regulated, both positively and negatively, by posttranslational histone modifications. For example, vernalization (the promotion of flowering by cold temperatures) epigenetically silences FLC expression through repressive histone modifications such as histone H3 lysine-9 dimethylation (H3K9me2) and H3K27me3. In contrast, an RNA polymerase II-associated complex (Paf1c) activates FLC expression through increased H3K4 and H3K36 methylation. As a result of this regulation, FLC has become a useful model for the study of chromatin structure in Arabidopsis. Here we show that At3g22590 is the Arabidopsis homolog of the yeast (Saccharomyces cerevisiae) Paf1c component CDC73 and is enriched at FLC chromatin. In contrast to other Paf1c component mutants that exhibit pleiotropic developmental phenotypes, the effects of cdc73 mutations are primarily limited to flowering time, suggesting that CDC73 may only be required for Paf1c function at a subset of target genes. In rapid-cycling strains, cdc73 mutants showed reduced FLC mRNA levels and decreased H3K4me3 at the FLC locus. Interestingly, in late-flowering autonomous-pathway mutants, which contain higher levels of FLC, cdc73 mutations only suppressed FLC in a subset of mutants. H3K4me3 was uniformly reduced in all autonomous-pathway cdc73 double mutants tested; however, those showing reduced FLC expression also showed an increase in H3K27me3. Thus, CDC73 is required for high levels of FLC expression in a subset of autonomous-pathway-mutant backgrounds and functions both to promote activating histone modifications (H3K4me3) as well as preventing repressive ones (e.g. H3K27me3).

journal_name

Plant Physiol

journal_title

Plant physiology

authors

Yu X,Michaels SD

doi

10.1104/pp.110.158386

subject

Has Abstract

pub_date

2010-07-01 00:00:00

pages

1074-84

issue

3

eissn

0032-0889

issn

1532-2548

pii

pp.110.158386

journal_volume

153

pub_type

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