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Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (RNA-seq)

ABSTRACT: Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (RNA-seq)

PROVIDER: PRJNA467529 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7132960.fastq.gz	Fastqsanger.gz
	SRR7132970.fastq.gz	Fastqsanger.gz
	SRR7132961.fastq.gz	Fastqsanger.gz
	SRR7132971.fastq.gz	Fastqsanger.gz
	SRR7132952.fastq.gz	Fastqsanger.gz

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Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (RNA-seq)

Project description:Basic helix-loop-helix (bHLH) proneural transcription factors (TFs) Ascl1 and Neurog2 are integral to the development of the nervous system. Here, we investigated the molecular mechanisms by which Ascl1 and Neurog2 control the acquisition of generic neuronal fate and impose neuronal subtype identity. Using direct neuronal programming of embryonic stem cells, we found that Ascl1 and Neurog2 regulate distinct targets by binding to largely different sets of sites. Their divergent binding pattern is not determined by the previous chromatin state but distinguished by specific E-box enrichments which reflect the DNA sequence preference of the bHLH domain. The divergent Ascl1 and Neurog2 binding patterns result in distinct chromatin accessibility and enhancer activity landscapes that shape the binding and activity of downstream TFs during neuronal specification. Our findings suggest that proneural factors contribute to neuronal diversity by differentially altering the chromatin landscapes that shape the binding of neuronally expressed TFs.

2019-02-27 | GSE114173 | GEO

Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (ChIP-seq)

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Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (ATAC-seq)

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Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2

Project description:Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2

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Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (single-cell RNA-seq)

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Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (ATAC-seq)

Project description:Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (ATAC-seq)

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Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (ChIP-seq)

Project description:Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (ChIP-seq)

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Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (single-cell RNA-seq)

Project description:Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (single-cell RNA-seq)

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Regulation of cortical folding by niche progenitor cells that co-express cross-repressive transcription factors Neurog2 and Ascl1

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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Proneural genes define ground state rules to regulate neurogenic patterning and cortical folding

Project description:Asymmetric neuronal expansion is thought to drive evolutionary transitions from lissencephalic to gyrencephalic cerebral cortices. We report that Neurog2 and Ascl1 proneural genes interact to sustain neurogenic continuity and lissencephaly in rodents. Using transgenic reporter mice and human cerebral organoids, we found that Neurog2 and Ascl1 expression defines a continuum of four lineage-biased neural progenitor cell (NPC) pools. Double+ NPCs, at the hierarchical apex, are least lineage-restricted due to Neurog2-Ascl1 cross-repression, and display unique features of multipotency (more open chromatin, complex gene regulatory network, G2 pausing). Strikingly, selective killing of double+ NPCs using Neurog2-Ascl1 split-Cre mice and three ‘deletor’ strains breaks neurogenic symmetry by locally disrupting Notch signaling, leading to cortical folding. Consistent with proneural genes driving discontinuous neurogenesis and folding via Notch, NEUROG2, ASCL1 and HES1 transcripts are modular in gyrencephalic macaque cortices. Neurog2/Ascl1 double+ NPCs are thus Notch-ligand expressing ‘niche’ cells that control neurogenic periodicity and cortical gyrification.

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