ArticleMolecular neurobiology2014
MGARP regulates mouse neocortical development via mitochondrial positioning.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
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- Transcriptional Responses of Different Brain Cell Types to Oxygen Decline.Brain sciences · 2024Article
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- Alterations in Retrotransposition, Synaptic Connectivity, and Myelination Implicated by Transcriptomic Changes Following Maternal Immune Activation in Nonhuman Primates.Biological psychiatry · 2021Article
- Mitochondria in Early Forebrain Development: From Neurulation to Mid-Corticogenesis.Frontiers in cell and developmental biology · 2021Review
- Glioma cells are resistant to inflammation‑induced alterations of mitochondrial dynamics.International journal of oncology · 2020Observational
- Neurodevelopmental impairment induced by prenatal valproic acid exposure shown with the human cortical organoid-on-a-chip model.Microsystems & nanoengineering · 2020Article
- Genetic cooperativity in multi-layer networks implicates cell survival and senescence in the striatum of Huntington's disease mice synchronous to symptoms.Bioinformatics (Oxford, England) · 2020Article
- Exploring the molecular interface between hypoxia-inducible factor signalling and mitochondria.Cellular and molecular life sciences : CMLS · 2019Review
- A genomic atlas of human adrenal and gonad development.Wellcome open research · 2017Article
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Authors and funding
5 authors.
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Abstract
Neocortical development is an extremely complicated process that critically depends on the proper migration, distribution, and positioning of neural cells. Here, we identified mitochondria-localized glutamic acid-rich protein (MGARP) as a negative regulator of neocortical development. In the developing neocortex, the overexpression of MGARP by in utero electroporation impedes the radial migration of neocortical cells to their final destination. These neocortical cells failed to be normally polarized, leading to shortened axons and compromised axonal bundles. The number of dendrites was also attenuated in cells with MGARP overexpression and was expanded in MGARP-knockdown or knockout cells. Mechanistic studies indicated that overexpression of MGARP caused alterations in the structural integrity, subcellular distribution, and motility of mitochondria. The mitochondria in MGARP-overexpressing cells became "fatty" with a round morphology, and the total number of mitochondria in MGARP-overexpressing cells was also decreased in the cell body and dendrites as well as in the axons. Time lapse studies showed that the ratio of motile mitochondria was remarkably decreased in the axons of MGARP-overexpressing cells. Together, our findings suggest that MGARP negatively mediates neocortical development by regulating mitochondrial distribution and motility in neocortical neurons.
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