| First Author | Di Bella DJ | Year | 2019 |
| Journal | Cell Rep | Volume | 28 |
| Issue | 9 | Pages | 2264-2274.e3 |
| PubMed ID | 31461644 | Mgi Jnum | J:284635 |
| Mgi Id | MGI:6385972 | Doi | 10.1016/j.celrep.2019.07.087 |
| Citation | Di Bella DJ, et al. (2019) Ascl1 Balances Neuronal versus Ependymal Fate in the Spinal Cord Central Canal. Cell Rep 28(9):2264-2274.e3 |
| abstractText | 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. |
