ArticleScientific reports2019
Role of Per3, a circadian clock gene, in embryonic development of mouse cerebral cortex.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
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- Physiological significance of WDR45, a responsible gene for β-propeller protein associated neurodegeneration (BPAN), in brain development.Scientific reports · 2021Article
- Comparative transcriptomic analysis of the brain in Takifugu rubripes shows its tolerance to acute hypoxia.Fish physiology and biochemistry · 2021Article
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- Neuroprotective Effects of Human Umbilical Cord-Derived Mesenchymal Stem Cells From Different Donors on Spinal Cord Injury in Mice.Frontiers in cellular neuroscience · 2021Article
- Circadian Regulation of Blood Pressure: of Mice and Men.Current hypertension reports · 2020Review
- Circadian Clock, Time-Restricted Feeding and Reproduction.International journal of molecular sciences · 2020Review
- Double UP: A Dual Color, Internally Controlled Platform forFrontiers in molecular neuroscience · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Per3 is one of the primary components of circadian clock system. While circadian dysregulation is known to be involved in the pathogenesis of several neuropsychiatric diseases. It remains largely unknown whether they participate in embryonic brain development. Here, we examined the role of clock gene Per3 in the development of mouse cerebral cortex. In situ hybridization analysis revealed that Per3 is expressed in the developing mouse cortex. Acute knockdown of Per3 with in utero electroporation caused abnormal positioning of cortical neurons, which was rescued by RNAi-resistant Per3. Per3-deficient cells showed abnormal migration phenotypes, impaired axon extension and dendritic arbor formation. Taken together, Per3 was found to play a pivotal role in corticogenesis via regulation of excitatory neuron migration and synaptic network formation.
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