Cortical and Commissural Defects Upon HCF-1 Loss in Nkx2.1-Derived Embryonic Neurons and Glia.

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Version: Final published version
License: CC BY 4.0
Serval ID
serval:BIB_96B5A3B59A2B
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Cortical and Commissural Defects Upon HCF-1 Loss in Nkx2.1-Derived Embryonic Neurons and Glia.
Journal
Developmental neurobiology
Author(s)
Minocha S., Herr W.
ISSN
1932-846X (Electronic)
ISSN-L
1932-8451
Publication state
Published
Issued date
06/2019
Peer-reviewed
Oui
Volume
79
Number
6
Pages
578-595
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
Formation of the cerebral cortex and commissures involves a complex developmental process defined by multiple molecular mechanisms governing proliferation of neuronal and glial precursors, neuronal and glial migration, and patterning events. Failure in any of these processes can lead to malformations. Here, we study the role of HCF-1 in these processes. HCF-1 is a conserved metazoan transcriptional co-regulator long implicated in cell proliferation and more recently in human metabolic disorders and mental retardation. Loss of HCF-1 in a subset of ventral telencephalic Nkx2.1-positive progenitors leads to reduced numbers of GABAergic interneurons and glia, owing not to decreased proliferation but rather to increased apoptosis before cell migration. The loss of these cells leads to development of severe commissural and cortical defects in early postnatal mouse brains. These defects include mild and severe structural defects of the corpus callosum and anterior commissure, respectively, and increased folding of the cortex resembling polymicrogyria. Hence, in addition to its well-established role in cell proliferation, HCF-1 is important for organ development, here the brain.
Keywords
Animals, Cerebral Cortex/embryology, Cerebral Cortex/metabolism, Cerebral Cortex/pathology, Corpus Callosum/embryology, Corpus Callosum/metabolism, Corpus Callosum/pathology, Female, Host Cell Factor C1/deficiency, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Neuroglia/metabolism, Neuroglia/pathology, Neurons/metabolism, Neurons/pathology, Pregnancy, Thyroid Nuclear Factor 1/metabolism, GABAergic neurons, Nkx2.1, anterior commissure, corpus callosum, cortex, glia, polymicrogyria
Pubmed
Web of science
Open Access
Yes
Create date
24/06/2019 17:55
Last modification date
15/01/2021 8:10
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