Biology Reference
In-Depth Information
AP1/SEP protein complex establishes sepal identity, while the AP1/SEP/AP3/PI complex specifies petal
identity [Theissen and Saedler, 2001]. At later stages of flower development, AP1/CAL is inhibited by
AGAMOUS (AG) in stamens and carpels [Gustafson-Brown
et al.
, 1994]. Since, according to the 'floral
quartet' model, the principal functional AG complexes in these floral organs are AG/SEP/AP3/PI and
AG/SEP, respectively, we assume in our model that both of these complexes can repress the expression
of
AP1
/
CAL
.
Genetic data and the results of gene expression microarray experiments suggest that LFY and AP1
positively regulate the expression of floral homeotic genes
AP3
,
PI
and
AG
[Huala and Sussex, 1992;
Weigel and Meyerowitz, 1993; Busch
et al.
, 1999; Honma and Goto, 2000; Lohmann
et al.
, 2001;
Wellmer
et al.
, 2006; Chae
et al.
, 2008].
For the upregulation of
AP3
and
PI
, LFY requires UNUSAL FLORAL ORGANS (UFO) as a cofactor
[Wilkinson and Haughn, 1995; Lee
et al.
, 1997]. LFY and UFO form functional protein complexes in
plants, which are required for binding of LFY to the promoter of
AP3
[Chae
et al.
, 2008]. The direct
binding of a LFY/UFO complex to the promoter of
PI
has not yet been demonstrated. However, since
LFY and UFO also activate
PI
expression via a common promoter region [Honma and Goto, 2000], we
assume in our model that the LFY/UFO complex acts in a similar manner on the
PI
promoter.
Floral homeotic genes. Aside from the initial activation by AP1 and LFY, there are two major aspects of
regulation of floral homeotic genes: (1) autoregulation via multiprotein complexes, and (2) the presence
of spatial factors that permit or prohibit the expression of floral homeotic genes in certain tissues within
the floral meristem. We implemented 3 known factors that spatially modulate homeotic gene expression:
(a) UFO, which is required together with LEAFY for the activation of
APETALA3
and
PISTILLATA
.
(b) APETALA2 (AP2), which negatively regulates
AG
in sepal and petal primordia [Drews
et al.
, 1991;
Bomblies
et al.
, 1999].
(c) SUPERMAN (SUP), which negatively regulates
AP3
and
PI
in carpel
primordia [Bowman
et al.
, 1992; Yun
et al.
, 2002].
The
SEPALLATA
genes (
SEP1
-
SEP4
) are closely related, highly redundant MADS-box genes which
are required for the specification of the identities of all types of floral organ due to upregulation of
other floral organ identity genes [Pelaz
et al.
, 2000; Ditta
et al.
, 2004]. Protein-protein interaction data
suggest that they form larger complexes with all other floral organ identity proteins belonging to the
MADS-box transcription factor family [Honma and Goto, 2001]. According to the current model of
flower development, each of the complexes is specific for a certain type of floral organ: the SEP/AP1
complex for sepals, the SEP/AP1/AP3/PI complex for petals, SEP/AG/AP3/PI for stamens and SEP/AG
for carpels (Fig. 1) [Honma and Goto, 2001; Theissen and Saedler, 2001]. Only little is known about
the regulation of SEP gene expression, however expression microarray data suggest that
SEP
genes
are activated by AP1/CAL, LFY and AG [Schmid
et al.
, 2003; Gomez-Mena
et al.
, 2005; Wellmer
et al.
, 2006]. There are several indications from genetic data that floral homeotic genes can positively
upregulate their own expression, and that SEP genes are required for this upregulation. AP3 and PI, which
act together in the specification of petal and stamen identity, depend on each other in the autoregulatory
process [Jack
et al.
, 1994]. Heterodimerization of the two gene products is required for the positive
autoregulation. Since also
SEP
,
AP1
(petals) and
AG
(stamen) gene products are able to upregulate of
AP3
and
PI
[Gustafson-Brown
et al.
, 1994; Pelaz
et al.
, 2000; Gomez-Mena
et al.
, 2005], we assume
in our model that the AP1/SEP/AP3/PI (petal) and AG/SEP/AP3/PI (stamen) protein complexes are the
functional complexes for upregulation of
AP3
and
PI in planta
.
Gomez-Mena
et al.
, 2005, demonstrated that AG can upregulate its own expression. Since both, the
AG
and
SEP
gene products can upregulate
AG
expression, and AG and SEP proteins can interact with
each other as well as with AP3 and PI in a higher-order protein complex [Honma and Goto, 2001], and
