|ZFIN ID: ZDB-PUB-200826-10|
Ascl1 Balances Neuronal versus Ependymal Fate in the Spinal Cord Central Canal
Di Bella, D.J., Carcagno, A.L., Bartolomeu, M.L., Pardi, M.B., Löhr, H., Siegel, N., Hammerschmidt, M., Marín-Burgin, A., Lanuza, G.M.
|Source:||Cell Reports 28: 2264-2274.e3 (Journal)|
|Registered Authors:||Hammerschmidt, Matthias, Löhr, Heiko, Siegel, Nicol|
|Keywords:||Ascl1, CSF-cN, CSF-contacting neurons, central canal, ependymocytes, late neurogenesis, neural progenitor, neuron specification, spinal cord, transcription factor|
|PubMed:||31461644 Full text @ Cell Rep.|
Di Bella, D.J., Carcagno, A.L., Bartolomeu, M.L., Pardi, M.B., Löhr, H., Siegel, N., Hammerschmidt, M., Marín-Burgin, A., Lanuza, G.M. (2019) Ascl1 Balances Neuronal versus Ependymal Fate in the Spinal Cord Central Canal. Cell Reports. 28:2264-2274.e3.
ABSTRACTGeneration 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.
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