The role of the lincRNA Pantr1 during the development of the neurons in the FOXG1 syndrome mouse model
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ABSTRACT:
PROVIDER: PRJNA722484 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14253300.fastq.gz | Fastqsanger.gz | |||
| SRR14253301.fastq.gz | Fastqsanger.gz | |||
| SRR14253302.fastq.gz | Fastqsanger.gz | |||
| SRR14253303.fastq.gz | Fastqsanger.gz | |||
| SRR14253284.fastq.gz | Fastqsanger.gz |
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Project description:This study instigates the role of the long non-coding RNA Pantr1 (or Brn1a) in the context of nervous system development and in the neurodevelopmental disorder Foxg1-related syndrome. We report a high-throughput single-end RNA sequencing experiment in hippocampal neurons cultured in vitro in mouse. We performed the knockdown of Purb, Pantr1 and Foxg1 in hippocampal neurons cultured in vitro to 7 days and performed RNA-seq analysis.
2025-05-21 | GSE172220 | GEO
Project description:Derailed gene expression programs within the developing nervous system, encompassing both transcriptional and posttranscriptional processes, are implicated in diverse neurodevelopmental diseases. One of those debilitating diseases, the FOXG1-syndrome, lacks full understanding of the mechanistic role of its eponymous gene product, FOXG1. While it is known that FOXG1 acts in part at the chromatin by binding to regulative regions, it is unclear what factors control its presence at specific sites. Long non-coding RNAs (lncRNAs) can mediate site-directed transcription factor binding, but their potential role in FOXG1-syndrome has not been described. Here, we show that the lncRNA Pantr1 mediates site specific binding of FOXG1 using FOXG1 ChIP sequencing upon Pantr1 knockdown.
2025-05-21 | GSE272852 | GEO
Project description:The lincRNA Pantr1 mediates site-specific chromatin binding of FOXG1 in hippocampal neurons
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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
Project description:Derailed gene expression programs within the developing nervous system, encompassing both transcriptional and posttranscriptional processes, can cause diverse neurodevelopmental diseases (NDD). The NDD FOXG1-syndrome lacks full understanding of the mechanistic role of its eponymous gene product. While it is known that FOXG1 acts in part at the chromatin by binding to regulative regions, it is unclear what factors control its presence at specific sites. Long non-coding RNAs (lncRNAs) can mediate site-directed transcription factor binding, but their potential role in FOXG1-syndrome has not been described. Here, we show that FOXG1 localisation is regulated at selected loci through the lncRNA Pantr1.
We identified FOXG1 as an upstream transcriptional activator of Pantr1 in human and mice. Further, we discovered that FOXG1 has the ability to associate with RNAs. Both, transcriptional regulation of Pantr1 by FOXG1 and association of both partners, build up a regulative network that impacts the localisation of FOXG1 at selected genomic loci. Specifically, Pantr1 facilitates cooperative presence of FOXG1/NEUROD1 at specific sites, and Pantr1 reduction leads to redistribution of FOXG1 to comparably more generic binding sites. The rescue of impaired dendritic outgrowth upon FOXG1 reduction by simultaneous overexpression of Pantr1 underlines the importance of the FOXG1/Pantr1 regulative network.
2025-04-15 | MSV000097630 | MassIVE
Project description:Derailed gene expression programs within the developing nervous system, encompassing both transcriptional and posttranscriptional processes, can cause diverse neurodevelopmental diseases (NDD). The NDD FOXG1-syndrome lacks full understanding of the mechanistic role of its eponymous gene product. While it is known that FOXG1 acts in part at the chromatin by binding to regulative regions, it is unclear what factors control its presence at specific sites. Long non-coding RNAs (lncRNAs) can mediate site-directed transcription factor binding, but their potential role in FOXG1-syndrome has not been described. Here, we show that FOXG1 localisation is regulated at selected loci through the lncRNA Pantr1.
We identified FOXG1 as an upstream transcriptional activator of Pantr1 in human and mice. Further, we discovered that FOXG1 has the ability to associate with RNAs. Both, transcriptional regulation of Pantr1 by FOXG1 and association of both partners, build up a regulative network that impacts the localisation of FOXG1 at selected genomic loci. Specifically, Pantr1 facilitates cooperative presence of FOXG1/NEUROD1 at specific sites, and Pantr1 reduction leads to redistribution of FOXG1 to comparably more generic binding sites. The rescue of impaired dendritic outgrowth upon FOXG1 reduction by simultaneous overexpression of Pantr1 underlines the importance of the FOXG1/Pantr1 regulative network.
2025-04-15 | MSV000097629 | MassIVE
Project description:The mouse model with Foxg1 frameshift mutation uncovers the pathophysiology of FOXG1 syndrome
| PRJNA935396 | ENA
Project description: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.
2019-10-22 | GSE106801 | GEO
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
Project description:To investigate the gene expression patterns in Foxg1 frameshift mutation, we performed RNAseq in P1 cortices of Q84Pfs heterozygote and littermate wild type control mice.
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