The distribution of the proteoglycan FORSE-1 in the developing mouse central nervous system.
FORSE-1
Lewis X
brain
development
mouse
spinal cord
Journal
Journal of anatomy
ISSN: 1469-7580
Titre abrégé: J Anat
Pays: England
ID NLM: 0137162
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
accepted:
11
10
2018
pubmed:
27
11
2018
medline:
20
6
2020
entrez:
27
11
2018
Statut:
ppublish
Résumé
Glycosylation is a major post-translational modification in which a carbohydrate known as a glycan is enzymatically attached to target proteins which regulate protein folding and stability. Glycans are strongly expressed in the developing nervous system where they play multiple roles during development. The importance of these glycan epitopes in neural development is highlighted by a group of conditions known as congenital disorders of glycosylation which lead to psychomotor difficulties, mental retardation, lissencephaly, microencephaly and epilepsy. One of these glycan epitopes, known as Lewis X, is recognised by the FORSE-1 antibody and is regionally expressed in the developing nervous system. In this study, we report the regional and temporal expression patterns of FORSE-1 immunolabelling during the periods of neurogenesis, gliogenesis and axonogenesis in developing mouse nervous system. We demonstrate the localisation of FORSE-1 on subsets of neuroepithelial cells and radial glial cells, and in compartments corresponding to axon tract formation. These spatial, temporal and regional expression patterns are suggestive of roles in the determination of different cell lineages and in the patterning of white matter during development, and help provide insights into the neuroanatomical regions affected by congenital disorders of glycosylation.
Identifiants
pubmed: 30474148
doi: 10.1111/joa.12907
pmc: PMC6326832
doi:
Substances chimiques
Antigens, Surface
0
Lewis X Antigen
0
antigen FORSE-1
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
216-226Informations de copyright
© 2018 Anatomical Society.
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