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Fig. 7. Instability of the stamen network assuming simple feedback. The presence of feedback loops of AP3/PI and AG to
their respective own genes and the fact that these assemble into a higher-order complex makes the network extremely sensitive
to differences in the production of the monomers. A) assuming standard parameters, the production of AG is slightly higher
than that of AP3/PI, the sequestering of AP3/PI by the SEP/AG complex leads to the collapse of its expression, causing a final
expression pattern corresponding to the carpel, with the accumulation of the SEP/AG complex. B) If the speed of AP3/PI
production is adjusted to be higher than that of AG, the expression of AG collapses leading to the accumulation of AP3/PI.
and robustness of the regulatory network, an attempt was made to rebuild the whole network so that the
autoregulatory links we redirected to start at their single monomers instead of protein complexes. In this
case the complexes were still produced as end products but they played no further role in regulation within
the network. Simulations were made following the same set of starting conditions as in the previous
model. While the correct steady state expression profiles for sepal, petal and carpel were observed (data
not shown), stable expression of the stamen complex was unattainable (Fig. 7). This was traced to the
presence of two separate positive autoregulatory feedback loops of the AP3/PI complex and AG acting
on the expression of their respective genes. Since AP3/PI and SEP/AG heterodimers assemble into
the higher-order SEP/AP3/PI/AG complex, the concentration of any free heterodimer depends on the
concentration of the other heterodimer. For instance, if the production of AG is higher than that of AP3
and PI, the SEP/AG dimer will bind to all the AP3/PI dimers available to form the higher-order complex,
and since AP3 and PI are positively autoregulated, the titration of the AP3/PI complex by SEP/AG will
lead to a decrease and eventual halt of the transcriptional activation of
AP3
and
PI
. This decrease in
AP3
and
PI
transcription causes formation of the carpel complex SEP/AG. On the other hand, if the
production speed of AP3 and PI is higher than that of AG, free AG, which under this assumption activates
its own expression, will be sequestered by SEP/AP3/PI and will be unable to activate its own expression,
leading to the loss of the stamen complex (Fig. 7). In this case feedback by the higher-order complex,
not by the single monomers, is a prerequisite in order to maintain a stable expression of the steady-state
transcription factor complex.
Extension of the network: Feedback loops controlling spatial regulators
Recently published ChIP-seq data [Kaufmann
et al.
, 2009] supports the idea that some of the spatial
patterning genes might be under feedback control from MADS-box transcription factor complexes. In
particular, binding of SEP3 to the promoters of
AP2
and three
miR172
orthologs suggest that SEP3
complexes (e.g. with AP1) could stabilize the expression of AP2 in the outer whorls and that other
SEP3 complexes might stabilize miR172 expression in the inner whorls. In order to test the feasibility
