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.