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CUT&RUN data of Chd4 and Mbd3 in mouse embryonic stem cells

ABSTRACT: This study investigates the role of ADNP in regulating CHD4 and MBD3 binding using CUT&RUN. CUT&RUN was performed to capture changes in the binding of CHD4 (using FLAG-tag) and MBD3. Two biological replicates were processed for each protein with two technical replicates. This dataset aims to characterise the binding of CHD4 and MBD3 in mouse ES cells.

INSTRUMENT(S): Illumina NovaSeq X

ORGANISM(S): Mus musculus

SUBMITTER: Brian Hendrich

PROVIDER: E-MTAB-15606 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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CUT&Tag data of MBD3 in mouse embryonic stem cells treated with auxin for CHD4 depletion against untreated control

Project description:This study investigates the effect of the chromatin remodeller CHD4 on MBD3 using CUT&Tag. CHD4 was tagged with a mini-AID degron to enable auxin-inducible degradation. CUT&Tag for MBD3 was performed at multiple time-points (4 hours and 24 hours) following auxin treatment vs untreated control (0 hours) to capture changes in MBD3 binding upon CHD4 depletion. For each time point, two biological replicates were processed.

2026-01-15 | E-MTAB-15627 | biostudies-arrayexpress

CUT&RUN data of Nanog and Sox2 in mouse embryonic stem cells treated with auxin for CHD4 depletion against untreated control

Project description:This study investigates the role of the chromatin remodeller CHD4 in regulating transcription factor binging using CUT&RUN. CHD4 was tagged with a mini-AID degron to enable auxin-inducible degradation. CUT&RUN for Nanog and Sox2 was performed at multiple time-points (30 minutes, 1 hour, and 4 hours) following auxin treatment to capture changes in their binding upon CHD4 depletion. For each time point, two biological replicates were processed, each with two technical replicates. This dataset aims to characterise the immediate effects of CHD4 loss on TF binding.

2026-01-15 | E-MTAB-15607 | biostudies-arrayexpress

CUT&Tag data of H3K27Ac and H3K4Me1 in mouse embryonic stem cells treated with auxin for CHD4 depletion against untreated control

Project description:This study investigates the effect of the chromatin remodeller CHD4 on H3K27Ac and H3K4Me1 using CUT&Tag. CHD4 was tagged with a mini-AID degron to enable auxin-inducible degradation. CUT&Tag for H3K27Ac and H3K4Me1 was performed at multiple time-points (4 hours and 24 hours) following auxin treatment vs untreated control (0 hours) to capture changes in histone modifications upon CHD4 depletion. For each time point, three biological replicates were processed.

2026-01-15 | E-MTAB-15625 | biostudies-arrayexpress

CUT&RUN data of Chd4 and Mbd3 in mouse embryonic stem cells

Project description:CUT&RUN data of Chd4 and Mbd3 in mouse embryonic stem cells

| PRJEB97812 | ENA

The ChAHP chromatin remodelling complex regulates a network of neurodevelopmental disorder risk genes to scale the production of neocortical layers (cut&run-seq)

Project description:Although chromatin remodellers are among the most important risk genes associated with neurodevelopmental disorders (NDDs), the roles of these complexes during brain development are in many cases unclear. Here, we focused on the recently discovered ChAHP chromatin remodelling complex. The zinc finger and homeodomain transcription factor ADNP is a core subunit of this complex, and de novo ADNP mutations lead to intellectual disability and autism spectrum disorder. However, germline Adnp knockout mice were previously shown to exhibit early embryonic lethality, obscuring subsequent roles for the ChAHP complex in neurogenesis. Here, we employed single cell transcriptomics, cut&run-seq, and histological approaches to characterize mice conditionally ablated for the ChAHP subunits Adnp and Chd4. We show that during neocortical development, Adnp and Chd4 orchestrate the production of late-born, upper-layer neurons through a two-step process. First, Adnp is required to sustain progenitor proliferation specifically during the developmental window for upper-layer cortical neurogenesis. Accordingly, we found that Adnp recruits Chd4 to genes associated with progenitor proliferation. Second, in postmitotic differentiated neurons, we define a network of risk genes linked to NDDs that are regulated by Adnp and Chd4. Taken together, these data demonstrate that ChAHP is critical for driving the expansion upper-layer cortical neurons, and for regulating neuronal gene expression programs, suggesting that these processes may potentially contribute to NDD etiology.

2024-12-29 | GSE255599 | GEO

ChAHP (Adnp, Chd4, HP1) mediates sequence-specific recruitment of HP1 independent of H3K9 methylation

Project description:Activity-dependent neuroprotective protein (ADNP) is one of the most frequent autism spectrum disorder-associated gene products known to date. Here we show that Adnp interacts with the chromatin remodeler Chd4 and the heterochromatin protein HP1 to form a stable complex, which we refer to as ChAHP. Genetic ablation of ChAHP components or DNA binding sites in embryonic stem cells prematurely activates lineage-specific genes, revealing an important role for Adnp in restraining the differentiation capacity of pluripotent cells. Adnp targets the ChAHP complex to specific sequence motifs at euchromatic loci, representing an H3K9 methylation-independent mechanism of HP1 recruitment and gene silencing.

2018-05-23 | GSE97945 | GEO

The nucleosome remodeling and deacetylase complex protein CHD4 regulates neural differentiation of mouse embryonic stem cells by down-regulating p53

Project description:Lineage specification of the three germ layers occurs during early embryogenesis and is critical for normal development. The nucleosome remodeling and deacetylase (NuRD) complex is a repressive chromatin modifier that plays a role in lineage commitment. However, the role of chromodomain helicase DNA-binding protein 4 (CHD4), one of the core subunits of the NuRD complex, in neural lineage commitment is poorly understood. Here, we report that the CHD4/NuRD complex plays a critical role in neural differentiation of mouse embryonic stem cells (ESCs). We found that RNAi-mediated Chd4 knockdown suppresses neural differentiation, as did knockdown of methyl-CpG binding domain protein Mbd3, another NuRD subunit. Chd4 and Mbd3 knockdowns similarly affected changes in global gene expression during neural differentiation and up-regulated several mesendodermal genes. However, inhibition of mesendodermal genes by knocking out the master regulators of mesendodemal lineages, Brachyury and Eomes, through a CRISPR/Cas9 approach could not restore the impaired neural differentiation caused by the Chd4 knockdown, suggesting that CHD4 controls neural differentiation not by repressing other lineage differentiation processes. Notably, Chd4 knockdown increased the acetylation levels of p53, resulted in increased protein levels of p53. Double knockdown of Chd4 and p53 restored the neural differentiation rate. Furthermore, overexpression of BCL2, a downstream factor of p53, partially rescued the impaired neural differentiation caused by the Chd4 knockdown. Our findings reveal that the CHD4/NuRD complex regulates neural differentiation of ESCs by down-regulating p53.

2018-11-07 | GSE114389 | GEO

The ChAHP chromatin remodelling complex regulates neurodevelopmental disorder risk genes to scale the production of neocortical layers

Project description:Although chromatin remodellers are among the most important risk genes associated with neurodevelopmental disorders (NDDs), the roles of these complexes during brain development are in many cases unclear. Here, we focused on the recently discovered ChAHP chromatin remodelling complex. The zinc finger and homeodomain transcription factor ADNP is a core subunit of this complex, andde novo ADNPmutations lead to intellectual disability and autism spectrum disorder. However, germlineAdnpknockout mice were previously shown to exhibit early embryonic lethality, obscuring subsequent roles for the ChAHP complex in neurogenesis. Here, we employed single cell transcriptomics, cut&run-seq, and histological approaches to characterize mice conditionally ablated for the ChAHP subunitsAdnpandChd4. We show that during neocortical development, Adnp and Chd4 orchestrate the production of late-born, upper-layer neurons through a two-step process. First, Adnp is required to sustain progenitor proliferation specifically during the developmental window for upper-layer cortical neurogenesis. Accordingly, we found that Adnp recruits Chd4 to genes associated with progenitor proliferation. Second, in postmitotic differentiated neurons, we define a network of risk genes linked to NDDs that are regulated by Adnp and Chd4. Taken together, these data demonstrate that ChAHP is critical for driving the expansion upper-layer cortical neurons, and for regulating neuronal gene expression programs, suggesting that these processes may potentially contribute to NDD etiology.

2024-12-30 | GSE262584 | GEO

Chd4 remodels chromatin to control retinal cell type specification and lineage termination

Project description:During development, neural progenitor cells modify their output over time to produce different types of neurons and glia in chronological sequences. Previous studies have shown that epigenetic processes play a crucial role in regulating neural progenitor potential, but the underlying mechanisms are not well understood. Here, we hypothesized that nucleosome remodelling would regulate the competence transitions of retinal progenitors. We generated retina-specific conditional knockouts (cKOs) in the key nucleosome remodelling enzyme Chd4. Chd4 cKOs overproduced early-born retinal ganglion and amacrine cells. Postnatally, later-born rod photoreceptors were drastically underproduced. Concomitantly, progenitors failed to be exhausted at late phases of development and ultimately overproduced Müller glia. To determine how Chd4 regulates the genome, we used cut&run-seq to reveal Chd4 genome occupancy, and ATAC-seq experiments to visualize nucleosome remodelling. These data revealed that genome accessibility was significantly increased at ∼10,000 regulatory elements and ∼4,000 genes in the Chd4 cKO. Together, these results suggest that Chd4 restricts the genome to repress progenitor identity and promote rod photoreceptor production. Accordingly, multiplexed single-cell transcriptomics demonstrated that deletion of Chd4 led to markedly divergent gene expression profiles. However, despite overproduction of early fates and underproduction of later-born rods, the perinatal transition between early and late progenitor competence was not altered as determined by birthdating experiments and transcriptomic signatures. Taken together, our data suggest that Chd4-dependent chromatin remodelling regulates cell fate specification, and is also required to terminate retinal neurogenesis, but that it does not regulate the progenitor competence windows that restrict early-vs. late-cell-type production.

2025-09-02 | GSE300175 | GEO

ChIP-seq of NuRD components and pluripotency factors in wild-type, Mbd3 and Sall4/1 mutant embryonic stem cells

Project description:Members of the Nucleosome Remodeling and Deacetylase (NuRD) complex Mbd3 and Mi2beta (Chd4) along with pluripotency regulators Nanog, Oct4, Klf4 and Esrrb were profiled for chromatin association by ChIP-seq in mouse embryonic stem cells mutant for Mbd3, Sall4 and/or the related Sall1 pluripotency-associated factors.

2016-08-09 | E-MTAB-4565 | biostudies-arrayexpress

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