PUBLICATION
Deletion of the chd7 Hinders Oligodendrocyte Progenitor Cell Development and Myelination in Zebrafish
- Authors
- Shi, L., Wang, Z., Li, Y., Song, Z., Yin, W., Hu, B.
- ID
- ZDB-PUB-230910-59
- Date
- 2023
- Source
- International Journal of Molecular Sciences 24(17): (Journal)
- Registered Authors
- Hu, Bing
- Keywords
- chd7, myelination, oligodendrocyte, zebrafish
- MeSH Terms
-
- Animals
- CHARGE Syndrome*/genetics
- Cell Differentiation/genetics
- DNA Helicases/genetics
- Oligodendrocyte Precursor Cells*
- Oligodendroglia
- Zebrafish/genetics
- PubMed
- 37686337 Full text @ Int. J. Mol. Sci.
Citation
Shi, L., Wang, Z., Li, Y., Song, Z., Yin, W., Hu, B. (2023) Deletion of the chd7 Hinders Oligodendrocyte Progenitor Cell Development and Myelination in Zebrafish. International Journal of Molecular Sciences. 24(17):.
Abstract
CHD7, an encoding ATP-dependent chromodomain helicase DNA-binding protein 7, has been identified as the causative gene involved in CHARGE syndrome (Coloboma of the eye, Heart defects, Atresia choanae, Retardation of growth and/or development, Genital abnormalities and Ear abnormalities). Although studies in rodent models have expanded our understanding of CHD7, its role in oligodendrocyte (OL) differentiation and myelination in zebrafish is still unclear. In this study, we generated a chd7-knockout strain with CRISPR/Cas9 in zebrafish. We observed that knockout (KO) of chd7 intensely impeded the oligodendrocyte progenitor cells' (OPCs) migration and myelin formation due to massive expression of chd7 in oilg2+ cells, which might provoke upregulation of the MAPK signal pathway. Thus, our study demonstrates that chd7 is critical to oligodendrocyte migration and myelination during early development in zebrafish and describes a mechanism potentially associated with CHARGE syndrome.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping