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Bcl6 neurogenic activity in in vitro cortical progenitors [RNA-Seq]

ABSTRACT: Bcl6 neurogenic activity in in vitro cortical progenitors [RNA-Seq]

PROVIDER: PRJNA549718 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9328981_1.fastq.gz	Fastqsanger.gz
	SRR9328981_2.fastq.gz	Fastqsanger.gz
	SRR9328982_1.fastq.gz	Fastqsanger.gz
	SRR9328982_2.fastq.gz	Fastqsanger.gz
	SRR9328983_1.fastq.gz	Fastqsanger.gz

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Bcl6 neurogenic activity in in vitro cortical progenitors [RNA-Seq]

Project description:Transcriptome analysis following Bcl6 induction (24h doxycycline) in mouse ES-cell-derived cortical progenitors (differentiation day 12) shows that Bcl6 promotes a neurogenic transcription program and represses selective genes of the main proliferative pathways.

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Bcl6 binding sites and neurogenic activity in in vitro cortical progenitors

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Bcl6 binding sites in in vitro cortical progenitors [ChIP-Seq]

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Bcl6 binding sites in in vitro cortical progenitors [ChIP-Seq]

Project description:Bcl6 binding sites in in vitro cortical progenitors [ChIP-Seq]

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Bcl6 binding sites and neurogenic activity in in vitro cortical progenitors

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2019-06-20 | GSE133032 | GEO

Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway II

Project description:Developmental neuron death plays a pivotal role in refining organization and wiring during neocortex formation. Aberrant regulation of this process results in neurodevelopmental disorders including impaired learning and memory. Underlying molecular pathways are incompletely determined. Loss of Bcl11a in cortical projection neurons induces pronounced cell death in upper-layer cortical projection neurons during postnatal corticogenesis. We used this genetic model to explore genetic mechanisms by which developmental neuron death is controlled. Unexpectedly, we found Bcl6, previously shown to be involved in transition of cortical neurons from progenitor to postmitotic differentiation state to provide a major check point regulating neuron survival during late cortical development. We show that Bcl11a is a direct transcriptional regulator of Bcl6. Deletion of Bcl6 exerts death of cortical projection neurons. In turn, reintroduction of Bcl6 into Bcl11a mutants prevents induction of cell death in these neurons. Together, our data identify a novel Bcl11a/Bcl6-dependent molecular pathway in regulation of developmental cell death during corticogenesis.

2022-06-24 | GSE185288 | GEO

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ERK signaling expands mammalian cortical radial glial cells and extends the neurogenic period

Project description:The molecular basis for cortical expansion during evolution remains largely unknown. Here, we report that fibroblast growth factor (FGF)-extracellular signal-regulated kinase (ERK) signaling promotes the self-renewal and expansion of cortical radial glial (RG) cells. Furthermore, FGF-ERK signaling induces bone morphogenic protein 7 (Bmp7) expression in cortical RG cells, which increases the length of the neurogenic period. We demonstrate that ERK signaling and Sonic Hedgehog (SHH) signaling mutually inhibit each other in cortical RG cells. We provide evidence that ERK signaling is elevated in cortical RG cells during development and evolution. We propose that the expansion of the mammalian cortex, notably in human, is driven by the ERK-BMP7-GLI3R signaling pathway in cortical RG cells, which participates in a positive feedback loop through antagonizing SHH signaling. We also propose that the relatively short cortical neurogenic period in mice is partly due to mouse cortical RG cells receiving higher SHH signaling that antagonizes ERK signaling.

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