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Nascent RNA-seq data of mouse embryonic stem cells treated with auxin for CHD4 depletion against untreated control

ABSTRACT: This study investigates the role of the chromatin remodeller CHD4 in regulating gene expression. CHD4 was tagged with a mini-AID degron to enable auxin-inducible degradation. RNA-seq of nascent transcripts was performed at multiple time-points (1, 2, 4 and 24 hours) following auxin treatment to capture changes in gene expression upon CHD4 depletion. For each time point, three biological replicates were processed. This dataset aims to characterise the immediate effects of CHD4 loss on gene expression.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Mus musculus

SUBMITTER: Brian Hendrich

PROVIDER: E-MTAB-15127 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RNA-seq data of 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 gene expression. CHD4 was tagged with a mini-AID degron to enable auxin-inducible degradation. RNA-seq was performed at multiple time-points (1, 2, 4 and 24 hours) following auxin treatment to capture changes in gene expression upon CHD4 depletion. For each time point, three biological replicates were processed. This dataset aims to characterise the immediate effects of CHD4 loss on gene expression.

2026-01-15 | E-MTAB-15102 | biostudies-arrayexpress

ATAC-seq data of mouse embryonic stem cells treated with auxin for CHD4 depletion against untreated control

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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.

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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.

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Defining the interactome of CHD4 in fusion-positive rhabdomyosarcoma

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2020-08-11 | PXD015231 | Pride

Expression data from glioblastoma cells after ZFHX4 or CHD4 suppression.

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ZFHX4 and CHD4 ChIP sequencing in glioblastoma tumor initiating cells

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2014-01-16 | E-GEOD-52419 | biostudies-arrayexpress

A regulatory role for CHD4 in maintenance of the spermatogonial stem cell pool

Project description:Maintenance and self-renewal of the spermatogonial stem cell (SSC) population is the cornerstone of male fertility. In this manuscript we have identified a key role for the nucleosome remodelling protein Chromodomain Helicase DNA binding protein 4 (CHD4) in regulating SSC function. Gene expression analyses revealed that CHD4 expression is largely restricted to spermatogonia in the mouse testis, and is particularly enriched in SSCs. Using spermatogonial transplantation techniques and RNAi mediated knockdown it was established that loss of Chd4 expression significantly impairs SSC regenerative capacity, resulting in a ~50% reduction in colonisation of recipient testes. A single cell RNA-seq comparison depicted reduced expression of ‘self-renewal’ genes such as Gfra1 and Pten following Chd4 knockdown, along with increased expression of signature progenitor genes, Neurog3 and Dazl. Co-immunoprecipitation analyses demonstrated that CHD4 regulates gene expression in spermatogonia not only though its traditional association with the remodelling complex NuRD, but also via interaction with the GDNF-responsive transcription factor SALL4. Cumulatively, the results of this study depict a previously unappreciated fundamental role for CHD4 in controlling fate decisions in the spermatogonial pool.

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The modulation of CHD4 nucleosome remodelling activity by auxiliary domains suggests unifies mechanistic aspects of chromatin remodelling across enzyme families

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