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Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE247087 | GEO | 2023/11/13

REPOSITORIES: GEO

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Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [RNA-Seq]

Project description:Epigenetic regulation is essential for the normal development of human cerebral cortex, and its disruptions would lead to diverse neurodevelopmental disorders. The epigenetic co-repressor CDYL exhibits widespread expression across various cell clusters within the human embryonic cortex, yet its roles in this intricate process have remained elusive. Here, we show that CDYL is critical for cortical neurogenesis, and CDYL deficiency led to an augmentation in the generation of GABAergic neurons instead of cortical progenitors and neurons in the cortical organoid model. Combining analysis of bulk RNA-seq and ChIP seq, we identified NNAT as a significant CDYL target by H3K27me3 modification, crucial for the fate determination of neural stem cells within human cortical organoids, distinctly diverging from the murine cortex at a similar developmental stage. Collectively, our study sheds light on the critical function of CDYL in the maintenance of cortical neural stem cell fate commitment during human corticogenesis through the inhibition of NNAT expression.

2023-11-13 | GSE247084 | GEO

Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [ChIP-Seq]

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Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT

Project description:Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT

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Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [RNA-Seq]

Project description:Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [RNA-Seq]

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Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [ChIP-Seq]

Project description:Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [ChIP-Seq]

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Chromodomain protein CDYL confers forebrain identity to human cortical organoids by inhibiting neuronatin [ChIP-seq]

Project description:Fate determination of neural stem cells is crucial for cerebral cortex development and is closely linked to neurodevelopmental disorders when gene expression networks are disrupted. The transcriptional corepressor chromodomain Y-like (CDYL) is widely expressed across diverse cell populations within the human embryonic cortex, though its precise role in this complex developmental process remains unclear. Here, we show that CDYL is critical for human cortical neurogenesis. CDYL deficiency leads to a substantial increase in gamma-aminobutyric acid (GABA)-ergic neurons in human cortical organoids, instead of the expected generation of typical cortical neurons. Subsequently, neuronatin (NNAT) is identified as a significant target of CDYL in this process, and its abnormal expression obviously influences the proliferation and fate commitment of cortical neural stem cells (NSCs) within human cortical organoids. Cross-species comparisons of CDYL targets unravel a distinct developmental trajectory between human cortical organoids and mouse cortex at an analogous stage. Collectively, our data provide insight into the evolutionary roles of CDYL in human cortex development, emphasizing the critical function of CDYL in maintaining the fate of human cortical NSCs.

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Chromodomain protein CDYL confers forebrain identity to human cortical organoids by inhibiting neuronatin [RNA-seq]

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The ciliary gene INPP5E confers dorsal telencephalic identity to human cortical organoids by negatively regulating Sonic hedgehog signaling.

Project description:Defects in primary cilia, cellular antennas that control multiple intracellular signaling pathways, underlie several neurodevelopmental disorders, but it remains unknown how cilia control essential steps in human brain formation. Here, we show that cilia are present on the apical surface of radial glial cells in human fetal forebrain. Interfering with cilia signaling in human organoids by mutating the INPP5E gene leads to the formation of ventral telencephalic cell types instead of cortical progenitors and neurons. INPP5E mutant organoids also show increased Sonic hedgehog (SHH) signaling, and cyclopamine treatment partially rescues this ventralization. In addition, ciliary expression of SMO, GLI2, GPR161, and several intraflagellar transport (IFT) proteins is increased. Overall, these findings establish the importance of primary cilia for dorsal and ventral patterning in human corticogenesis, indicate a tissue-specific role of INPP5E as a negative regulator of SHH signaling, and have implications for the emerging roles of cilia in the pathogenesis of neurodevelopmental disorders.

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Specification of positional identity in forebrain organoids.

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Chromodomain protein CDYL confers forebrain identity to human cortical organoids by inhibiting neuronatin [ChIP-seq]

Project description:Chromodomain protein CDYL confers forebrain identity to human cortical organoids by inhibiting neuronatin [ChIP-seq]

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