Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA268486 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1662315.fastq.gz | Fastqsanger.gz | |||
| SRR1662316.fastq.gz | Fastqsanger.gz | |||
| SRR1662317.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
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Project description:The abscence of TBR2 gene in human leads to microcephaly. This condition is mimicked by the specific ablation of the murine gene in developing cerebral cortex. Herein we compared gene expression in control and Tbr2 cKO in E14.5 cerebral cortices. This approach represents a useful tool to identify the molecular mechanisms at the basis of the phenotype. 6 samples, 3x Tbr2 +/+;Foxg1::Cre (control) and 3x Tbr2 fl/fl;Foxg1::Cre
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Project description:Humans exemplify gyrencephalic species with folded cerebral cortices, contrasting with lissencephalic mammals such as mice. Here we investigated how proneural genes Neurog2 and Ascl1 control cortical folding by regulating neurogenic patterns. Cortical neural progenitor cells (NPCs) stratify into four pools (proneural negative, Neurog2+, Ascl1+, double+) that are distributed evenly in mouse cortices and modular in gyrencephalic macaque cortices and pseudo-folded human cerebral organoids. Each pool has distinct developmental potentials, transcriptomes, epigenomes, and gene regulatory networks. Neurog2-Ascl1 form a bistable toggle switch double+ NPCs to prevent lineage commitment observed in single+ NPCs. Neurog2 and Ascl1 act redundantly to control neurogenic timing, with NPCs precociously depleted in Neurog2-/-;Ascl1-/- cortices. Finally, selective killing of Neurog2/Ascl1 double+ NPCs using Neurog2/Ascl1 split-Cre;Rosa-DTA transgenics breaks neurogenic symmetry in mice by locally disrupting Notch signaling, leading to cortical folding. Our findings suggest that Neurog2/Ascl1 double+ NPCs are Notch-ligand expressing ‘niche’ cells that regulate neurogenic continuity and cortical gyrification.
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Project description:To date, speculations on the molecular roles of Tbr2 transcription factor during specification, maintenance and differentiation of cortical specific Intermediate Neural Progenitors are coming from the analysis of loss- and gain-of-function experiments. However since its capacity to bind the DNA to extert its function we did Chromatin Immuno-Precipitation followed by deep sequencing to profile its target on the genome. We performed this approach directly in vivo to respect the physiological and peculiar enviroment of its action during cortical development. Moreover we did the same approach for Neurogenin 2 proneural gene. Interestingly the vast majority of the Neurog2 peaks are in common with Tbr2 dataset suggesting a co-operation between the two factors confirmed by biochemical and functional assays. Finally we compared Tbr2 dataset with the DNA regions bound by the H3K27me3 histone demethylase Jmjd3 (NCBI:Kdm6b) obtained by others. Interestingly we were able to find regions in common linked to important genes for neuronal differentiation. 3 samples, one input chromatin, one ChIP for Tbr2 and one ChIP for Neurog2
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Project description:The neocortex is comprised of six neuronal layers that are derived in an inside-out sequence. Neurog2, a proneural gene encoding a basic-helix-loop-helix transcription factor, is required and sufficient to specify the fate of only early-born, deep-layer neurons, despite being expressed throughout the cortical neurogenic period. To identify potential inhibitors of Neurog2 function, we used a TAP-tagging screen, identifying L3mbtl3, a histone methyl-lysine binding protein that interacts with Rnf2 in Polycomb Repressive Complex 1 (PRC1), as a novel Neurog2 interactor. We found that L3mbtl3 is co-expressed with Neurog2 and other PRC1 genes in cortical progenitors. In L3mbtl3 knock-out (KO) cortices, upper-layer neurons are generated in reduced numbers, and instead, the cortical progenitor pool is expanded. Transcriptomic analyses of L3mbtl3 KO cortices at early and mid neurogenesis revealed a striking upregulation of negative regulators of transcription, including Rest, a repressor of many neurogenic genes, and an associated downregulation of neuronal differentiation and maturation genes. Notably, transcriptomic changes occur in the absence of any changes to chromatin structure, suggesting that L3mbtl3 influences gene transcription directly and not via changes to the chromatin. Instead, L3mbtl3 represses Neurog2 transcriptional activity in vitro and blocks cortical progenitor cell maturation and neuronal migration in vivo by altering the expression of scaffold genes. L3mbtl3 is thus an essential negative regulator of cortical neurogenesis.
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