Staufen 1 is expressed by neural precursor cells in the developing murine cortex but is dispensable for NPC self-renewal and neuronal differentiation in vitro
Autor: | C.A. Kuc, J.P. Vessey, H.H.A. Thorpe, J.T. Brott, A. Smart |
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Rok vydání: | 2021 |
Předmět: |
Cytoplasm
Cell division Neurogenesis RNA-binding protein Hippocampal formation Biology Mice 03 medical and health sciences 0302 clinical medicine Neural Stem Cells Cortex (anatomy) medicine Animals Molecular Biology 030304 developmental biology Cell Nucleus Cerebral Cortex Neurons 0303 health sciences General Neuroscience RNA-Binding Proteins Cell biology medicine.anatomical_structure Cerebral cortex Neurology (clinical) Neuron Nucleus 030217 neurology & neurosurgery Developmental Biology |
Zdroj: | Brain Research. 1773:147700 |
ISSN: | 0006-8993 |
DOI: | 10.1016/j.brainres.2021.147700 |
Popis: | Background Proper development of the cerebral cortex relies on asymmetric divisions of neural precursor cells (NPCs) to produce a recurring NPC and a differentiated neuron. Asymmetric divisions are promoted by the differential localization of cell-fate determinants, such as mRNA, between daughter cells. Staufen 1 (Stau1) is an RNA-binding protein known to localize mRNA in mature hippocampal neurons. Its expression pattern and role in the developing mammalian cortex remains unknown. Results Both stau1 mRNA and Stau1 protein were found to be expressed in all cells of the developing murine cortex. Stau1 protein expression was characterized spatially and temporally throughout cortical development and found to be present in all stages investigated. We observed expression in the nucleus, cytoplasm and distal processes of both NPCs and newly born neurons and found it to shuttle between the nucleus and the cytoplasm. Upon shRNA-mediated knock-down of Stau1 in primary cultures of the developing cortex, we did not observe any phenotype in NPCs. They were able to both self-renew and generate neurons in the absence of Stau1 expression. Conclusions We propose that Stau1 is either dispensable for the development of the cerebral cortex or that its paralogue, Stau2, is able to compensate for its loss. |
Databáze: | OpenAIRE |
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