ArticleCerebral cortex (New York, N.Y. : 1991)2019
Foxg1 Regulates the Postnatal Development of Cortical Interneurons.
Article in Cerebral cortex (New York, N.Y. : 1991), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- FOXG1 Transcriptionally Orchestrates ParvalbuminNeuroscience bulletin · 2026Article
- Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons.Nature communications · 2025Article
- The patient-specific mouse model with Foxg1 frameshift mutation provides insights into the pathophysiology of FOXG1 syndrome.Nature communications · 2025Article
- GABA/Glutamate Neuron Differentiation Imbalance and Increased AKT/mTOR Signaling in CNTNAP2Biological psychiatry global open science · 2025Article
- PAK3 activation promotes the tangential to radial migration switch of cortical interneurons by increasing leading process dynamics and disrupting cell polarity.Molecular psychiatry · 2024Article
- Menin Deficiency Induces Autism-Like Behaviors by Regulating Foxg1 Transcription and Participates in Foxg1-Related Encephalopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The molecular basis of p21-activated kinase-associated neurodevelopmental disorders: From genotype to phenotype.Frontiers in neuroscience · 2023Review
- FOXG1 sequentially orchestrates subtype specification of postmitotic cortical projection neurons.Science advances · 2022Article
- Early Deletion ofFrontiers in cell and developmental biology · 2022Article
- Cerebral organoids as tools to identify the developmental roots of autism.Molecular autism · 2020Review
- PDK1 regulates the survival of the developing cortical interneurons.Molecular brain · 2020Article
- Early ear neuronal development, but not olfactory or lens development, can proceed without SOX2.Developmental biology · 2020Article
- Disruption of Foxg1 impairs neural plasticity leading to social and cognitive behavioral defects.Molecular brain · 2019Article
- Bi-modal reprogramming of cell cycle by MiRNA-4673 amplifies human neurogenic capacity.Cell cycle (Georgetown, Tex.) · 2019Article
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8 authors at 2 institutions in 1 country.
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Abstract
Abnormalities in cortical interneurons are closely associated with neurological diseases. Most patients with Foxg1 syndrome experience seizures, suggesting a possible role of Foxg1 in the cortical interneuron development. Here, by conditional deletion of Foxg1, which was achieved by crossing Foxg1fl/fl with the Gad2-CreER line, we found the postnatal distributions of somatostatin-, calretinin-, and neuropeptide Y-positive interneurons in the cortex were impaired. Further investigations revealed an enhanced dendritic complexity and decreased migration capacity of Foxg1-deficient interneurons, accompanied by remarkable downregulation of Dlx1 and CXCR4. Overexpression of Dlx1 or knock down its downstream Pak3 rescued the differentiation detects, demonstrated that Foxg1 functioned upstream of Dlx1-Pak3 signal pathway to regulate the postnatal development of cortical interneurons. Due to the imbalanced neural circuit, Foxg1 mutants showed increased seizure susceptibility. These findings will improve our understanding of the postnatal development of interneurons and help to elucidate the mechanisms underlying seizure in patients carrying Foxg1 mutations.
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