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The dual origin, structural organization, and evolving ascending stratification of the mammalian neocortex are explored from a developmental perspective. Layer I and subplate (layer VII) zone of the neocortex evolve first from a primordial plexiform neuropil that is established throughout the non-olfactory telencephalon and that is common to amphibians, reptiles and mammals. The remaining laminations (strata) of the neocortex evolve later, between layer I and the subplate zone, from the cortical plate (CP), which represents a multilayered mammalian evolutionary feature. The attraction of CP neurons towards layer I, their progressive ascending (inside-out) placement, common early differentiation stage (regardless of size, location, cortical depth, or eventual functional role, or all of these), and the unique morphologic features of its pyramidal neuron are developmental processes controlled by layer I and its Cajal-Retzius cells. based on the role of these early neurons and of layer I, a new theory of neocortical cytoarchitectonics and nomenclature is proposed to explain the basic structural and functional organization of the mammalian neocortex, the morphology of its pyramidal cells, and the addition of new pyramidal cell strata that characterize its phylogenetic evolution.

The Cbfb gene, the non-DNA-binding subunit of the heterodimeric core-binding factor (CBF), is essential for embryogenesis. Specifically, it is found to be required for CBF(alpha)2 function in vivo. Homozygous mutation of the Cbfb gene is found to result in the same range of abnormalities observed in Cbfa2-deficient mice, including embryonic lethality at midgestation due to hemorrhaging in the central nervous system and inhibition of fetal liver hematopoiesis.

The CBFB-MYH11 gene was introduced into mouse genome by inserting the 3' part of the human MYH11 cDNA into the end of exon 5 of the mouse Cbfb gene through homologous recombination. This led to the creation of a half genomic (Cbfb), half cDNA (MYH11) fusion gene, which, in turn, resulted in the generation of a Cbf(beta)-SMMHC fusion protein under the control of the Cbfb promoter. Cbf(beta)-SMMHC is shown to dominantly suppress the normal function of Cbf gene products and inhibits the differentiation of hematopoietic stem cells.