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

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

PROVIDER: PRJNA1156626 | ENA |

REPOSITORIES: ENA

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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]

| PRJNA1156625 | ENA

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.

2024-09-18 | GSE276321 | GEO

Chromodomain protein CDYL confers forebrain identity to human cortical organoids by inhibiting neuronatin [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.

2024-09-18 | GSE276320 | GEO

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

| PRJNA1036200 | ENA

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

2023-11-13 | GSE247086 | GEO

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

2023-11-13 | GSE247084 | GEO

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]

| PRJNA1036193 | ENA

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]

| PRJNA1036206 | ENA

CDYL ChIP-Seq in mouse hippocampus

Project description:Here we report that the epigenetic factor Chromodomain Y-like (CDYL) protein is a critical regulator for the initiation and maintenance of activity-dependent intrinsic neuroplasticity. Genome-wide ChIP-sequencing analysis revealed that CDYL regulates multiple neuronal functional pathways including voltage-gated ion channels in mouse brains. We showed that CDYL binds to a regulatory element in the intron region of SCN8A and mainly recruits H3K27me3 activity for transcriptional repression of the gene. Injection of lentivirally-delivered CDYL shRNA to rat hippocampal neurons resulted in augmented Nav1.6-mediated sodium currents, lower neuronal threshold and increased seizure susceptibility, whereas transgenic mice over-expressing CDYL had higher neuronal threshold and were less prone to epileptogenesis. Finally, examination of human brain tissues revealed decreased expression of CDYL and increased expression of SCN8A in the temporal lobe epilepsy group. Together, our findings indicate CDYL is a critical player for experience-dependent gene regulation in controlling intrinsic excitability, which potentially contributes to learning and memory and CNS disorders involving change in activity such as epilepsy.

2017-06-25 | GSE96721 | GEO

Biological significance of CDYL in endometrial receptivity

Project description:Impaired endometrial receptivity is one of the major causes of recurrent implantation failure (RIF), and the underlying molecular mechanism has not been fully elucidated. We demonstrated that Chromodomain Y like (CDYL) was highly expressed in the endometrium at mid-secretory phase during the normal menstrual cycles. However, the expression of CDYL was down-regulated in the endometrial tissues obtained from women with RIF, consistently with the protein level of LIF, which is the marker of endometrial receptivity. Knockdown of CDYL significantly decreased the cell migration of human endometrial Ishikawa cells and primary endometrial cells. Genomic analyses revealed that CDYL gene silencing resulted in decreased expression of many genes associated with cytoskeleton and migration regulation.

2020-09-28 | GSE141239 | GEO

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