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The classical view of mammalian cortical development suggests that pyramidal neurons are generated in a temporal sequence, with all radial glial cells (RGCs) contributing to both lower and upper neocortical layers. A recent opposing proposal suggests there is a subgroup of fate-restricted RGCs in the early neocortex, which generates only upper-layer neurons. Little is known about the existence of fate restriction of homologous progenitors in other vertebrate species. We investigated the lineage of selected Emx2+ [vertebrate homeobox gene related to Drosophila empty spiracles (ems)] RGCs in mouse neocortex and chick forebrain and found evidence for both sequential and fate-restricted programs only in mouse, indicating that these complementary populations coexist in the developing mammalian but not avian brain. Among a large population of sequentially programmed RGCs in the mouse brain, a subset of self-renewing progenitors lack neurogenic potential during the earliest phase of corticogenesis. After a considerable delay, these progenitors generate callosal upper-layer neurons and glia. On the other hand, we found no homologous delayed population in any sectors of the chick forebrain. This finding suggests that neurogenic delay of selected RGCs may be unique to mammals and possibly associated with the evolution of the corpus callosum.

Original publication

DOI

10.1073/pnas.1506377112

Type

Journal article

Journal

Proc Natl Acad Sci U S A

Publication Date

08/09/2015

Volume

112

Pages

E5058 - E5067

Keywords

Emx2, chick, cortical development, neocortex, neurogenesis, Animals, Brain, Chick Embryo, Chickens, Corpus Callosum, Ependymoglial Cells, Green Fluorescent Proteins, Homeodomain Proteins, Luminescent Proteins, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Confocal, Neocortex, Neural Stem Cells, Neurogenesis, Neuroglia, Neurons, Prosencephalon, Transcription Factors