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Fig. 7. Model. (A) Multipotent cortical progenitors harbor a
cell-autonomous program in which, by asymmetric divisions, they become
progressively restricted in developmental potential. At an early stage of
corticoneurogenesis (around E10 in mice) they produce reelin-positive CR
neurons followed by deep-layer and outer-layer pyramidal neurons and
eventually macroglia [modified from Mizutani and Gaiano
(Mizutani and Gaiano, 2006)].
The transcription factor Foxg1 appears to function as a constitutive active
molecular switch required for early fate transitions in asymmetric
proliferating precursors (i.e. by suppressing the production of
reelin-positive CR neurons). (B) Ectopic expression of Zbtb20 in
immature cortical pyramidal neurons leads to hippocampus-like neurogenesis of
these cells apparently without affecting the early generation of CR neurons.
The hippocampus-like transformations involved a deficiency in neurons
expressing deep-layer (i.e. ER81) and outer-layer markers (i.e. Brn-1 and
Brn-2) in Zbtb20 transgenic brains. The model suggests that Zbtb20 represses
cell fate transitions in newborn pyramidal neurons and orchestrates the
invariant morphogenesis of these neurons. The differentiation of macroglia
from late precursors was not investigated in this work.
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