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FoxG1 function in hippocampus

ABSTRACT: The forkhead box transcription factor FoxG1 is known to influence forebrain development by determining regional brain specification as well as by regulating expansion of neuronal progenitors and timing of their differentiation. In the adult brain, FoxG1 is expressed in cortex and hippocampus. In the latter it is involved in postnatal neurogenesis in the dentate gyrus by influencing maintenance of the progenitor pool as well as survival and maturation of postmitotic neurons. In humans, haploinsufficiency of FoxG1 causes the congenital version of the Rett syndrome, a progressive neurologic developmental disorder. We use FoxG1 mutant mice to screen for global changes in mRNA expression after partial loss of FoxG1 protein in hippocampi of six week-old mice. Data analysis points to a specific function for FoxG1 in adult hippocampus besides its known involvement in dentate gyrus neurogenesis. We analyse transcriptional changes in the different CA-fields and show that especially the CA-1 field is influenced by lack of FOXG1 protein. Furthermore, data analysis shows altered expression of genes that have also been implicated in the classical form of the Rett syndrome and other autism spectrum disorders.

ORGANISM(S): Mus musculus

PROVIDER: GSE106801 | GEO | 2019/10/22

REPOSITORIES: GEO

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Identification of FOXG1 interaction partners

Project description:Rett syndrome is a complex neurodevelopmental disorder that is mainly caused by mutations in MECP2. However, mutations in FOXG1 cause a less frequent non-congenital form called atypical Rett syndrome. FOXG1 is a key transcription factor implicated in forebrain development, where it maintains the balance between progenitor proliferation and neuronal differentiation. Using SILAC based quantitative proteomics and genome-wide small RNA sequencing, we identified that FOXG1 interacts with the ATP-dependent RNA helicase, DDX5/p68 and controls the biogenesis of miRNAs. Both, FOXG1 and DDX5 bind to the miR200b/a/429 primary transcript and associate with the microprocessor complex, whereby DDX5 recruits FOXG1 to DROSHA. In vivo and in vitro experiments show that both FOXG1 and DDX5 are necessary for effective maturation of miR200b/a/429. RNAseq analyses of Foxg1-heterozygote hippocampi and miR200b/a/429 overexpressing Neuro-2a cells revealed that the cAMP-dependent protein kinase type II-beta regulatory subunit (PRKAR2B) is a target of miR200 in neural cells. Since it is known that PRKAR2B inhibits postsynaptic functions by attenuating protein kinase A (PKA) activity, increased PRKAR2B levels may contribute to neuronal dysfunctions in FOXG1 Rett syndrome.

2019-11-11 | PXD007040 | Pride

Differential vulnerability of adult neurogenic niches to dosage of the Neurodevelopmental-disorder linked gene FoxG1

Project description:We report that the two adult neurogenic niches of the mammalian brain – the dentate gyrus of the hippocampal formation and the subependymal zone of the lateral ventricles - displayed differential vulnerability to increased FoxG1 dosage: high FoxG1 levels severely compromised survival and glutamatergic dentate granule neuron fate acquisition in the hippocampal neurogenic niche, but left neurogenesis of GABAergic neurons in the subependymal zone / olfactory bulb system unaffected. Comparative transcriptomic analyses revealed a significantly higher expression of the apoptosis-linked nuclear receptor Nr4a1 in FoxG1-overexpressing hippocampal neural precursors. Our results reveal differential vulnerability of neuronal subtypes to increased FoxG1 dosage and suggest that activity of a FoxG1/Nr4a1 axis contributes to such subtype-specific response.

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FOXG1 drives transcriptomic networks to specify principal neuron subtypes during the development of the medial pallium

Project description:The medial pallium (MP) is the major forebrain region underlying learning and memory, spatial navigation, and emotion; however, the mechanisms underlying the specification of its principal neuron subtypes remain largely unexplored. Here, by postmitotic deletion of FOXG1 (a transcription factor linked to autism and FOXG1 syndrome) and single-cell RNA sequencing, we found that FOXG1 controls the specification of upper-layer retrosplenial cortical pyramidal neurons (RSC-PyNs (UL)), subiculum PyNs (SubC-PyNs), CA1-PyNs, CA3-PyNs and dentate gyrus granule cells (DG-GCs) in the mouse MP. We uncovered subtype-specific and subtype-shared FOXG1-regulated transcriptomic networks orchestrating MP neuron specification.

2022-10-19 | GSE215356 | GEO

FOXG1 and DDX5 control PRKAR2B expression via miR200 in a mouse model of atypical Rett-syndrome

Project description:Rett syndrome is a complex neurodevelopmental disorder that is mainly caused by mutations in MECP2. However, mutations in FOXG1 cause a less frequent non-congenital form called atypical Rett syndrome. FOXG1 is a key transcription factor implicated in forebrain development, where it maintains the balance between progenitor proliferation and neuronal differentiation. Using quantitative proteomics and genome-wide small RNA sequencing, we identified that FOXG1 interacts with the ATP-dependent RNA helicase, DDX5/p68 and controls the biogenesis of miRNAs. Both, FOXG1 and DDX5 bind to the miR200b/a/429 primary transcript and associate with the microprocessor complex, whereby DDX5 recruits FOXG1 to DROSHA. In vivo and in vitro experiments show that both FOXG1 and DDX5 are necessary for effective maturation of miR200b/a/429. RNAseq analyses of Foxg1-heterozygote hippocampi and miR200b/a/429 overexpressing Neuro-2a cells revealed that the cAMP-dependent protein kinase type II-beta regulatory subunit (PRKAR2B) is a target of miR200 in neural cells. Since it is known that PRKAR2B inhibits postsynaptic functions by attenuating protein kinase A (PKA) activity, increased PRKAR2B levels may contribute to neuronal dysfunctions in FOXG1 Rett syndrome.

2019-09-22 | GSE104169 | GEO

miR200 family target gene identification in Neuro2A cells

Project description:Rett syndrome is a complex neurodevelopmental disorder that is mainly caused by mutations in MECP2. However, mutations in FOXG1 cause a less frequent non-congenital form called atypical Rett syndrome. FOXG1 is a key transcription factor implicated in forebrain development, where it maintains the balance between progenitor proliferation and neuronal differentiation. Using quantitative proteomics and genome-wide small RNA sequencing, we identified that FOXG1 interacts with the ATP-dependent RNA helicase, DDX5/p68 and controls the biogenesis of miRNAs. Both, FOXG1 and DDX5 bind to the miR200b/a/429 primary transcript and associate with the microprocessor complex, whereby DDX5 recruits FOXG1 to DROSHA. In vivo and in vitro experiments show that both FOXG1 and DDX5 are necessary for effective maturation of miR200b/a/429. RNAseq analyses of Foxg1-heterozygote hippocampi and miR200b/a/429 overexpressing Neuro-2a cells revealed that the cAMP-dependent protein kinase type II-beta regulatory subunit (PRKAR2B) is a target of miR200 in neural cells. Since it is known that PRKAR2B inhibits postsynaptic functions by attenuating protein kinase A (PKA) activity, increased PRKAR2B levels may contribute to neuronal dysfunctions in FOXG1 Rett syndrome.

2019-10-22 | GSE106802 | GEO

Transcriptome analysis of single cells from the mouse dentate gyrus [10X]

Project description:RNA sequencing was performed on 5454 single cells from dentate gyrus of CD-1 mice, sampled at postnatal day 12, 16, 24 and 35, with the aim of studying the postnatal dentate gyrus neurogenesis.

2017-12-13 | GSE95315 | GEO

Single-Cell Analysis of Aging Mouse Dentate Gyrus

Project description:The dentate gyrus of the hippocampus is a brain region involved in learning, memory formation, and spatial coding. We performed single-cell RNA-sequencing of the dentate gyrus of young and old mice to identify the age-induced changes.

2023-07-19 | GSE205936 | GEO

Transcriptome analysis of single cells from the developing mouse dentate gyrus

Project description:RNA sequencing was performed on 24185 single cells from dentate gyrus of CD-1, C57Bl/6, or hGFAP-GFP reporter mice, sampled at ages ranging from embryonal day 16.5 to postnatal day 132, with the aim of comparing peri- and postnatal neurogenesis in the dentate gyrus

2017-12-13 | GSE104323 | GEO

Next-generation sequencing facilitates quantitative analysis of the transcriptomes of FOXG1 100% dosage, FOXG1 60% dosage, FOXG1 30% dosage, and FOXG1 0% dosage GABA interneurons derived from human embryonic stem cells

Project description:Next-generation sequencing facilitates quantitative analysis of the transcriptomes of FOXG1 100% dosage GABA interneurons, FOXG1 60% dosage GABA interneurons, FOXG1 30% dosage GABA interneurons, and FOXG1 0% dosage GABA interneurons derived from human embryonic stem cells. We report a genetic manipulation system that enable precise dosage control of FOXG1 protein in human pluripotent stem cells (hPSCs). Using this system, we explored how the various reduced dosage affect human ventrol GABA interneuron development. We employed RNA seq on hPSC-derived GABA interneurons (day 60) to invest the expression pattern under different FOXG1 dosage conditions. RNA-Seq on GABA interneurons (Day 60) indicates that compared to the FOXG1 100% group, variable insufficiency of FOXG1 produces more than 1000 differently expressed genes (DEGs), and more DEGs in the group with less FOXG1 dosage. Heat map on Pearson Correlation indicates that groups with more discriminated FOXG1 exhibit much weaker correlation. Venn diagram reveals that each group has a set of distinct DEGs, suggesting that each FOXG1 protein dosage could results in different expression pattern during differentiation. The DEGs can be divided into two clusters, with one showing dosage-dependent regulation by FOXG1 and the other one typical binary. Key regulatory genes for GABA interneuron induction (NKX2-1, NKX6-2, GAD1, etc.) and for functional GABAergic-speciﬁc synapse formation (GABBR1, GABRA1, GABRB1, GABRG1, GABRQ, SHANK1, etc.) are down regulated along with reduction of FOXG1 protein.

2018-09-18 | GSE120079 | GEO

A ketogenic diet rescues hippocampal memory defects in a mouse model of Kabuki syndrome

Project description:Kabuki syndrome is a Mendelian intellectual disability syndrome caused by mutations in either of two genes (KMT2D and KDM6A) involved in chromatin accessibility. We previously showed that an agent that promotes chromatin opening, the histone deacetylase inhibitor (HDACi) AR-42, ameliorates the deficiency of adult neurogenesis in the granule cell layer of the dentate gyrus, and rescues hippocampal memory defects in a mouse model of Kabuki syndrome (Kmt2d+/βGeo). Unlike a drug, a dietary intervention could be quickly transitioned to the clinic. Therefore, we have explored whether treatment with a ketogenic diet could lead to a similar rescue through increased amounts of beta-hydroxybutyrate, an endogenous HDACi. Here, we report that a ketogenic diet in Kmt2d+/βGeo mice modulates H3ac and H3K4me3 in the granular cell layer, with concomitant rescue of both the neurogenesis defect and hippocampal memory abnormalities seen in Kmt2d+/βGeo mice; similar effects on neurogenesis were observed upon exogenous administration of beta-hydroxybutyrate. These data suggests that dietary modulation of epigenetic modifications through elevation of beta-hydroxybutyrate may provide a feasible strategy to treat the intellectual disability seen in Kabuki syndrome and related disorders. We used microarrays to query global gene expression changes in the hippocampus of wild type and Kmt2d+/βGeo (Kabuki syndrome model) mice on a regular diet to identify specific gene expression abnormalities in the hippocampus of the Kabuki syndrome mouse model.

2016-12-03 | GSE90836 | GEO

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