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Multimodal epigenetic changes and altered NEUROD1 chromatin binding in the mouse hippocampus underlie FOXG1 syndrome

ABSTRACT: The data presented in this study enlighten for the first time in a comprehensive manner diverse and multi-modal functions of FOXG1 at the chromatin level in mature neurons. Despite FOXG1 being recognized as a key transcription factor for telencephalic development and neuronal function, insights into the mechanism underlying transcriptional regulation are sparse. We here show that (i) FOXG1 acts both as repressor and activator, (ii) localizes predominantly to enhancer regions, (iii) alters the epigenetic landscape, (iv) affects directly HDAC functions, and (v) acts in concert with NEUROD1 to instruct transcriptional programs necessary for axono- and synaptogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE189118 | GEO | 2023/01/09

REPOSITORIES: GEO

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Multimodal epigenetic changes and altered NEUROD1 chromatin binding in the mouse hippocampus underlie FOXG1 syndrome

Project description:The data presented in this study enlighten for the first time in a comprehensive manner diverse and multi-modal functions of FOXG1 at the chromatin level in mature neurons. Despite FOXG1 being recognized as a key transcription factor for telencephalic development and neuronal function, insights into the mechanism underlying transcriptional regulation are sparse. We here show that (i) FOXG1 acts both as repressor and activator, (ii) localizes predominantly to enhancer regions, (iii) alters the epigenetic landscape, (iv) affects directly HDAC functions, and (v) acts in concert with NEUROD1 to instruct transcriptional programs necessary for axono- and synaptogenesis.

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Multimodal epigenetic changes and altered NEUROD1 chromatin binding in the mouse hippocampus underlie FOXG1 syndrome

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Multimodal epigenetic changes and altered NEUROD1 chromatin binding in the mouse hippocampus underlie FOXG1 syndrome

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Multimodal epigenetic changes and altered NEUROD1 chromatin binding in the mouse hippocampus underlie FOXG1 syndrome

Project description:We report that FOXG1 localises at promoter, distal intergenic and intronic regions in vitro.The data presented in this study enlighten for the first time in a comprehensive manner diverse and multi-modal functions of FOXG1 at the chromatin level in mature neurons. Despite FOXG1 being recognized as a key transcription factor for telencephalic development and neuronal function, insights into the mechanism underlying transcriptional regulation are sparse. We here show that (i) FOXG1 acts both as repressor and activator, (ii) localizes predominantly to enhancer regions, (iii) alters the epigenetic landscape, (iv) affects directly HDAC functions, and (v) acts in concert with NEUROD1 to instruct transcriptional programs necessary for axono- and synaptogenesis.

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Multimodal epigenetic changes and altered NEUROD1 chromatin binding in the mouse hippocampus underlie FOXG1 syndrome

Project description:As part of our multimodal investigation fo FOXG1 functions at the chromatin, we report that there are both increase and decrease in chromatin accessibility upon reduced levels of FOXG1 in pirmary hippocampal neurons. The data presented in this study enlighten for the first time in a comprehensive manner diverse and multi-modal functions of FOXG1 at the chromatin level in mature neurons. Despite FOXG1 being recognized as a key transcription factor for telencephalic development and neuronal function, insights into the mechanism underlying transcriptional regulation are sparse. We here show that (i) FOXG1 acts both as repressor and activator, (ii) localizes predominantly to enhancer regions, (iii) alters the epigenetic landscape, (iv) affects directly HDAC functions, and (v) acts in concert with NEUROD1 to instruct transcriptional programs necessary for axono- and synaptogenesis.

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Multimodal epigenetic changes and altered NEUROD1 chromatin binding in the mouse hippocampus underlie FOXG1 syndrome

Project description:The integrative and multi-omics view of changes upon FOXG1 reduction reveals an unprecedented multimodality of FOXG1 functions converging on neuronal maturation, fueling novel therapeutic options based on epigenetic drugs to alleviate, at least in part, neuronal dysfunctions. This RNA-seq dataset is part of tis multimodal invetigation of FOXG1 functions.

2023-01-09 | GSE189117 | GEO

Multimodal epigenetic changes and altered NEUROD1 chromatin binding in the mouse hippocampus underlie FOXG1 syndrome

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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

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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.

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2022-03-02 | PXD005072 | Pride

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