Publications by authors named "Melanie Lebel-Potter"

Article Synopsis
  • Researchers used targeted mouse alleles of the Ascl1 gene to study cerebellum circuit formation, marking all glial and neuron types from the ventricular zone using genetic inducible fate mapping (GIFM).
  • Each cell type exhibited a unique timing in marking with Ascl1, allowing for the birth dating of specific neuron types like Purkinje cells and GABAergic interneurons during embryonic development.
  • Ascl1 is essential for generating most ventricle zone-derived cells; its absence leads to decreased interneurons and an imbalance in oligodendrocytes and astrocytes, indicating its critical role in neuron positioning and the development of cerebellar circuits.
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Proneural genes such as Ascl1 are known to promote cell cycle exit and neuronal differentiation when expressed in neural progenitor cells. The mechanisms by which proneural genes activate neurogenesis--and, in particular, the genes that they regulate--however, are mostly unknown. We performed a genome-wide characterization of the transcriptional targets of Ascl1 in the embryonic brain and in neural stem cell cultures by location analysis and expression profiling of embryos overexpressing or mutant for Ascl1.

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Background: While the diversity and spatio-temporal origin of olfactory bulb (OB) GABAergic interneurons has been studied in detail, much less is known about the subtypes of glutamatergic OB interneurons.

Results: We studied the temporal generation and diversity of Neurog2-positive precursor progeny using an inducible genetic fate mapping approach. We show that all subtypes of glutamatergic neurons derive from Neurog2 positive progenitors during development of the OB.

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Little is known of the intracellular machinery that controls the motility of newborn neurons. We have previously shown that the proneural protein Neurog2 promotes the migration of nascent cortical neurons by inducing the expression of the atypical Rho GTPase Rnd2. Here, we show that another proneural factor, Ascl1, promotes neuronal migration in the cortex through direct regulation of a second Rnd family member, Rnd3.

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