Loss of O-GlcNAc transferase in neural stem cells impairs corticogenesis
Autor: | Yan Wu, Fengjiao Liu, Juanxian Cheng, Liping Chen, Minghe Huang, Jingyuan Shao, Ying Li, Ming Fan, Haitao Wu |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Male Biophysics Apoptosis Biology Hippocampal formation N-Acetylglucosaminyltransferases Biochemistry 03 medical and health sciences 0302 clinical medicine Neural Stem Cells medicine Morphogenesis Transferase Animals Molecular Biology Cerebral Cortex Mice Knockout Neurons Endoplasmic reticulum Multipotent Stem Cells Cell Biology Dendrites Endoplasmic Reticulum Stress Embryonic stem cell Neural stem cell Axons Cell biology Corticogenesis 030104 developmental biology medicine.anatomical_structure nervous system Cerebral cortex 030220 oncology & carcinogenesis Disks Large Homolog 4 Protein |
Zdroj: | Biochemical and biophysical research communications. 532(4) |
ISSN: | 1090-2104 |
Popis: | The proper development of the cerebral cortex is essential for brain formation and functioning. O-GlcNAcylation, an important posttranslational modification, regulates the pathways critical for neuronal health and the survival of the cerebral cortex in neurodegenerative diseases. However, the role of O-GlcNAcylation in regulating cerebral cortical development at the embryonic and early postnatal (0-21 days) stages is still largely unknown. Here we report that the selective deletion of O-GlcNAc transferase (OGT) in neural stem cells (NSCs) in mice led to a series of severe brain developmental deficits, including dramatic shrinkage of cortical and hippocampal histoarchitecture, widespread neuronal apoptosis, decrease in cell proliferation, induction of endoplasmic reticulum (ER) stress, and inhibition of neuronal dendritic and axonal differentiation. The pathology of corticogenesis deficits caused by OGT deletion may largely rely on complicated biological processes, such as proliferation, apoptosis and differentiation. Our results suggest that dysfunctional O-GlcNAcylation in NSCs may be an important contributor to neurodevelopmental diseases. |
Databáze: | OpenAIRE |
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