| Literature DB >> 33871356 |
Laura Morcom1, Ilan Gobius1, Ashley Pl Marsh2,3, Rodrigo Suárez1, Jonathan Wc Lim1, Caitlin Bridges1, Yunan Ye1, Laura R Fenlon1, Yvrick Zagar4, Amelia M Douglass1, Amber-Lee S Donahoo1, Thomas Fothergill1, Samreen Shaikh1, Peter Kozulin1, Timothy J Edwards1,5, Helen M Cooper1, Elliott H Sherr6, Alain Chédotal4, Richard J Leventer3,7,8, Paul J Lockhart2,3, Linda J Richards1,9.
Abstract
The forebrain hemispheres are predominantly separated during embryogenesis by the interhemispheric fissure (IHF). Radial astroglia remodel the IHF to form a continuous substrate between the hemispheres for midline crossing of the corpus callosum (CC) and hippocampal commissure (HC). Deleted in colorectal carcinoma (DCC) and netrin 1 (NTN1) are molecules that have an evolutionarily conserved function in commissural axon guidance. The CC and HC are absent in Dcc and Ntn1 knockout mice, while other commissures are only partially affected, suggesting an additional aetiology in forebrain commissure formation. Here, we find that these molecules play a critical role in regulating astroglial development and IHF remodelling during CC and HC formation. Human subjects with DCC mutations display disrupted IHF remodelling associated with CC and HC malformations. Thus, axon guidance molecules such as DCC and NTN1 first regulate the formation of a midline substrate for dorsal commissures prior to their role in regulating axonal growth and guidance across it.Entities:
Keywords: agenesis of the corpus; astrocyte morphology; callosum; deleted in colorectal cancer; developmental biology; human; interhemispheric fissure remodelling; midline zipper glia; mouse; neuroscience; telencephalic development
Mesh:
Substances:
Year: 2021 PMID: 33871356 PMCID: PMC8116049 DOI: 10.7554/eLife.61769
Source DB: PubMed Journal: Elife ISSN: 2050-084X Impact factor: 8.713