Agriculture Reference
In-Depth Information
flowering-time genes (Putterill
et al.
, 1995; Robson
et al.
, 2001), and is discussed in
more detail in Section 7.2.3.2. This pathway probably also plays a role in the effect
of light quality on flowering, because high ratios of far-red to red light promote
flowering and stabilize the CO protein (Valverde
et al.
, 2004), although the flowering
response to light quality also involves a CO-independent pathway (Cerdan & Chory,
2003).
A second genetic pathway controls the response to vernalization. In response
to extended exposures to low temperature, this pathway reduces the abundance of
the mRNA encoding the MADS box transcription factor FLC, which is a potent re-
pressor of flowering (Michaels & Amasino, 1999; Sheldon
et al.
, 1999). Therefore,
vernalization accelerates flowering by reducing
FLC
expression. The autonomous
pathway also regulates
FLC
expression (Sheldon
et al.
, 2000; Michaels & Amasino,
2001). Mutations in a third pathway, the autonomous pathway, delay flowering under
both long and short days, and cause an increase in
FLC
mRNA levels. This pathway
regulates
FLC
expression independently of vernalization, so that the late flowering
caused by mutations in this pathway and the high
FLC
mRNA levels observed in
these mutants can be corrected by vernalization. Mutants affected in this pathway
also show an altered flowering-time in response to ambient temperatures (Blazquez
et al.
, 2003). The autonomous pathway appears to represent protein complexes in-
volved in histone modification and RNA processing (Simpson
et al.
, 2003; Ausin
et al.
, 2004), and probably also has a more general role than the regulation of
FLC
expression. Finally, the growth regulator gibberellic acid (GA) promotes flower-
ing of
Arabidopsis
, and mutations that affect genes required for GA biosynthesis
delay flowering, particularly under short days (Wilson
et al.
, 1992). This general
framework of three interacting pathways that promote flowering of
Arabidopsis
in
the absence of vernalization is supported by the observation that a triple mutant
carrying the
co
mutation (impairs the photoperiod pathway), the
ga1
mutation (re-
duces GA synthesis) and the
fca
mutation (impairs the autonomous pathway) never
flowered under long days (Reeves & Coupland, 2001).
These distinct genetic pathways converge to regulate the expression of a small
group of downstream genes, sometimes described as floral integrators (Mouradov
et al.
, 2002; Simpson & Dean, 2002). This group contains three genes, two of which
promote flowering,
FLOWERING LOCUS T
(
FT
) and
SUPPRESSOR OF OVER-
EXPRESSION OF CO 1
(
SOC1
), and a third,
LEAFY
, that encodes a transcription
factor required to confer floral identity on developing floral primordia.
FT
encodes
a protein with similarity to RAF kinase inhibitors of animals (Kardailsky
et al.
,
1999; Kobayashi
et al.
, 1999), and is discussed in more detail in the following
section, whereas
SOC1
encodes a MADS box transcription factor (Borner
et al.
,
2000; Lee
et al.
, 2000; Samach
et al.
, 2000). Mutations in each of these genes delay
flowering, whereas their overexpression from the viral CaMV 35S promoter causes
extreme early flowering. The expression of
SOC1
and
FT
is increased by CO and
reduced by FLC, indicating that they are downstream of the point of convergence of
the vernalization and photoperiod pathways (Samach
et al.
, 2000; Hepworth
et al.
,
2002). Furthermore, the expression of
SOC1
is increased by treating plants with
GA, suggesting that it acts downstream of all three pathways (Moon
et al.
, 2003).
