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Fig. 11. A comparison of GRN architecture in the large micromere-PMC lineage and
NSM cells. In presumptive PMCs (left), maternal ß-catenin activates
pmar1, which represses hesC. Components of the MAPK
signaling pathway are activated in the PMC lineage by an unknown mechanism and
bring about the phosphorylation and activation of Ets1/2. Ets1/2 and
alx1 regulate genes that control ingression, migration, and
biomineralization, and alx1 has an essential input into PMC
signaling. Note that although snail is a transcriptional repressor,
it stimulates ingression (Wu and McClay,
2007). In presumptive NSM cells (right), several components of the
PMC GRN (e.g. ets1/2, delta and snail) are
normally expressed, although little is known concerning their upstream
regulators. MAPK signaling is active and presumably causes the phosphorylation
of Ets1/2. Alx1 and tbr are normally repressed, directly or
indirectly, by the PMC-derived signal (genes not normally expressed in NSM
cells are shown in brackets). Key downstream targets of alx1 in the
skeletogenic pathway are therefore not expressed. Elimination of the signal
induces expression of alx1, which is sufficient to engage all
essential, missing elements of the PMC GRN. One consequence of the activation
of the PMC GRN in NSM cells is the acquisition of PMC-specific signaling
properties (Ettensohn and Ruffins,
1993).
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