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Fig. 3. Model for the regulation of the floral repressor FLC throughout
the Arabidopsis life cycle. During seedling growth, a group of genes
encode proteins that function as activators of FLC expression (shown
in purple); these genes include FRI, FRL1, FRL2, ESD4, ART1, PIE1,
VIP3 and VIP4. These proteins may maintain FLC
chromatin in an active state (indicated by an open structure and the presence
of active histone tail modifications shown in green). The autonomous pathway
functions antagonistically to the activators to repress FLC
expression. The RNA-binding proteins FCA, FPA and FLK, and the polyadenylation
factor FY, may function post-transcriptionally to achieve this and are shown
in red. The FVE/FLD proteins act with a putative histone deacetylase (HDAC;
all shown in orange) to promote an inactive FLC chromatin state,
represented by a closed structure with inactive histone tail modifications
(red). FLC is also repressed by exposure to long periods of cold
(vernalization). The proteins acting in the vernalization pathway are shown in
pink. Prolonged cold induces VIN3 expression, which promotes an
inactive FLC chromatin state. Subsequently, the VRN1 and VRN2
proteins are recruited to FLC, and are required for the methylation
of FLC histones and the maintenance of silencing. These marks may
promote the association of silencing factors with FLC chromatin that
reinforce its repression. During meiosis, gametogenesis or early
embryogenesis, FLC repression is overcome, thus resetting its
expression in the next generation.
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