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A conserved differentiation program facilitates inhibitory neuron production in the developing mouse and human cerebellum

ABSTRACT: A conserved differentiation program facilitates inhibitory neuron production in the developing mouse and human cerebellum

PROVIDER: PRJNA1236373 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32701072.fastq.gz	Fastqsanger.gz
	SRR32701073.fastq.gz	Fastqsanger.gz
	SRR32701074.fastq.gz	Fastqsanger.gz
	SRR32701075.fastq.gz	Fastqsanger.gz
	SRR32701076.fastq.gz	Fastqsanger.gz

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A conserved differentiation program facilitates inhibitory neuron production in the developing mouse and human cerebellum

Project description:Understanding the molecular mechanisms driving lineage decisions and differentiation during development is especially difficult in systems with a diverse progenitor pool, such as the mammalian cerebellum. Here, we used single-cell RNA-sequencing (scRNA-seq) to characterise the developmental trajectories of Nestin-expressing progenitors (NEPs) in the neonatal mouse cerebellum. We identified FOXO1 as a key regulator of NEP-to-inhibitory neuron differentiation, acting directly downstream of ASCL1. Genome occupancy and functional genomic experiments using primary NEPs showed that both ASCL1 and FOXO1 regulate neurogenesis genes during in vitro differentiation, while independently regulating proliferation and survival, respectively. Furthermore, we demonstrate that WNT is a regulator of the transition from an ASCL1+ to FOXO1+ state. Finally, we show that the ASCL1-FOXO1 axis and role of WNT signalling is conserved in primary human NEPs. Through understanding how cerebellar interneurons differentiate, our findings may inform therapeutic strategies for cerebellar disorders such as spinocerebellar ataxia, where cerebellar interneurons are overproduced.

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The imbalance of excitatory/inhibitory neuron differentiation in neurodevelopmental disorders with an NR2F1 point mutation

Project description:Recent studies have revealed an essential role for embryonic cortical development in the pathophysiology of neurodevelopmental disorders, including autism spectrum disorder (ASD). However, the genetic basis and underlying mechanisms remain unclear. Here, we generate mutant human embryonic stem cell lines (Mut hESCs) carrying an NR2F1-R112K mutation that has been identified in a patient with ASD features, and investigate their neurodevelopmental alterations. Mut hESCs overproduce ventral telencephalic neuron progenitors (ventral NPCs) and inhibitory neurons, and underproduce dorsal NPCs and excitatory neurons. These alterations can be mainly attributed to the aberrantly activated Hedgehog signaling pathway. Moreover, the corresponding Nr2f1 point mutant mice display a similar excitatory/inhibitory neuron imbalance and abnormal behaviors. Antagonizing the increased inhibitory synaptic transmission partially alleviates their behavioral deficits. Together, our results suggest that the NR2F1-dependent imbalance of excitatory/inhibitory neuron differentiation caused by the activated Hedgehog pathway is one precursor of neurodevelopmental disorders and may enlighten the therapeutic approaches.

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The identification and tumorigenecity of neuronal progenitors in developing cerebellum

Project description:It is generally believed that cerebellar granule neurons originate exclusively from granule neuron precursors (GNPs) in the external germinal layer (EGL). Here we identify a rare population of neuronal progenitors in the developing cerebellum that expresses Nestin. Although Nestin is widely considered a marker for multipotent stem cells, these Nestin-expressing progenitors (NEPs) are committed to the granule neuron lineage. Unlike conventional GNPs, which reside in the outer EGL and proliferate extensively, NEPs reside in the deep part of the EGL and are quiescent. Expression profiling reveals that NEPs are distinct from GNPs, and in particular, express markedly reduced levels of genes associated with DNA repair. Consistent with this, upon aberrant activation of Sonic hedgehog (Shh) signaling, NEPs exhibit more severe genomic instability and give rise to tumors more efficiently than GNPs. These studies identify a novel progenitor for cerebellar granule neurons and a novel cell of origin for medulloblastoma.

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Spatial enhancer activation influences inhibitory neuron identity during mouse embryonic development

Project description:Spatial enhancer activation influences inhibitory neuron identity during mouse embryonic development

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Spatial enhancer activation influences inhibitory neuron identity during mouse embryonic development

Project description:Spatial enhancer activation influences inhibitory neuron identity during mouse embryonic development

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The imbalance of excitatory/inhibitory neuron differentiation in neurodevelopmental disorders with an NR2F1 point mutation (The Third Replicate)

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The identification and tumorigenecity of neuronal progenitors in developing cerebellum

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RNA Sequencing of postnatal mouse Math1-Cre; Sufu flox/- cerebellum

Project description:Transcriptional profiling to identify genes differentially regulated by Sufu during cerebellum development. Sufu was specifically deleted from the granule neuron compartment using Math1-driven Cre recombinase.

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Spatial enhancer activation determines inhibitory neuron identity (ChIP-seq of MEIS transcription factors)

Project description:Spatial enhancer activation determines inhibitory neuron identity (ChIP-seq of MEIS transcription factors)

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A Functionally Conserved Gene Regulatory Network Module Governing Olfactory Neuron Diversity

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