info:eu-repo/semantics/article
Ascl1 Balances Neuronal versus Ependymal Fate in the Spinal Cord Central Canal
Fecha
2019-08Registro en:
Di Bella, Daniela Jesica; Carcagno, Abel Luis; Bartolomeu, M. Lucía; Pardi, Belén; Löhr, Heiko; et al.; Ascl1 Balances Neuronal versus Ependymal Fate in the Spinal Cord Central Canal; Elsevier; Cell Reports; 28; 9; 8-2019; 2264-2274.e3
2211-1247
CONICET Digital
CONICET
Autor
Di Bella, Daniela Jesica
Carcagno, Abel Luis
Bartolomeu, M. Lucía
Pardi, Belén
Löhr, Heiko
Siegel, Nicole
Hammerschmidt, Matthias
Marin Burgin, Antonia
Lanuza, Guillermo Marcos
Resumen
Generation of neuronal types at the right time, location, and number is essential for building a functional nervous system. Significant progress has been reached in understanding the mechanisms that govern neuronal diversity. Cerebrospinal fluid-contacting neurons (CSF-cNs), an intriguing spinal cord central canal population, are produced during advanced developmental stages, simultaneous with glial and ependymal cells. It is unknown how CSF-cNs are specified after the neurogenesis-to-gliogenesis switch. Here, we identify delayed Ascl1 expression in mouse spinal progenitors during the gliogenic phase as key in CSF-cN differentiation. With fate mappings and time-controlled deletions, we demonstrate that CSF-cNs derive from Ascl1-expressing cells and that Ascl1 triggers late neurogenesis in the amniote spinal cord. Ascl1 abrogation transforms prospective CSF-cN progenitors into ependymocytes. These results demonstrate that late spinal progenitors have the potential to produce neurons and that Ascl1 initiates CSF-cN differentiation, controlling the precise neuronal and nonneuronal composition of the spinal central canal.