Repurposing of the multiciliation gene regulatory network in fate specification of Cajal-Retzius neurons
[EN] Cajal-Retzius cells (CRs) are key players in cerebral cortex development, and they display a unique transcriptomic identity. Here, we use scRNA-seq to reconstruct the differentiation trajectory of mouse hem-derived CRs, and we unravel the transient expression of a complete gene module previousl...
| Autores: | , , , , , , , , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión aceptada para publicación |
| Fecha de publicación: | 2023 |
| País: | España |
| Institución: | Ajuntament de Barcelona |
| Repositorio: | BULERIA. Repositorio Institucional de la Universidad de León |
| OAI Identifier: | oai:buleria.unileon.es:10612/23632 |
| Acceso en línea: | https://www.sciencedirect.com/science/article/pii/S1534580723002459?via%3Dihub https://hdl.handle.net/10612/23632 |
| Access Level: | acceso abierto |
| Palabra clave: | Biología Biotecnología Genética Cajal-Retzius cells Cerebral cortex Multiciliogenesis Neuronal differentiation Neuronal identity Fate specification Choroid plexus 2407 Biología Celular 3109.02 Genética 24 Ciencias de la Vida 240108 Genética Animal 240701 Cultivo Celular 2409 Genética 2415 Biología Molecular |
| Sumario: | [EN] Cajal-Retzius cells (CRs) are key players in cerebral cortex development, and they display a unique transcriptomic identity. Here, we use scRNA-seq to reconstruct the differentiation trajectory of mouse hem-derived CRs, and we unravel the transient expression of a complete gene module previously known to control multiciliogenesis. However, CRs do not undergo centriole amplification or multiciliation. Upon deletion of Gmnc, the master regulator of multiciliogenesis, CRs are initially produced but fail to reach their normal identity resulting in their massive apoptosis. We further dissect the contribution of multiciliation effector genes and identify Trp73 as a key determinant. Finally, we use in utero electroporation to demonstrate that the intrinsic competence of hem progenitors as well as the heterochronic expression of Gmnc prevent centriole amplification in the CR lineage. Our work exemplifies how the co-option of a complete gene module, repurposed to control a distinct process, may contribute to the emergence of novel cell identities |
|---|