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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [RNA-seq]

ABSTRACT: To establish the role of Chd4 on controlling gene expression programs in the beta cell, we generated a tamoxifen-inducible, beta-cell-specific knockout mouse model; control (MIP-CreERT; Chd4flox/+;R26RtdTomato) and Chd4Db (MIP-CreERT; Chd4flox/flox;R26RtdTomato.

ORGANISM(S): Mus musculus

PROVIDER: GSE217445 | GEO | 2023/05/31

REPOSITORIES: GEO

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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [ATAC-seq]

Project description:To establish the role of Chd4 on controlling gene expression programs in the beta cell, we generated a tamoxifen-inducible, beta-cell-specific knockout mouse model; control (MIP-CreERT; Chd4flox/+;R26RtdTomato) and Chd4Db (MIP-CreERT; Chd4flox/flox;R26RtdTomato.

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The effect of TGF-beta in Apc-mutated mouse intestinal organoids

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Effect of fbw7 deletion in mouse pancreatic ducts

Project description:The adult pancreas is capable of limited regeneration after injury, but has no defined stem cell population. The cell types and molecular signals that govern the production of new pancreatic tissue are not well understood. Here we show that inactivation of the SCF-type E3 ubiquitin ligase substrate recognition component Fbw7 induces pancreatic ductal cells to reprogram into β-cells. The induced β-cells resemble islet β-cells in morphology and histology, express genes essential for β-cell function, and release insulin upon glucose challenge. Thus, loss of Fbw7 appears to reawaken an endocrine developmental differentiation program in adult pancreatic ductal cells. Our study highlights the plasticity of seemingly differentiated adult cells, identifies Fbw7 as a master regulator of cell fate decisions in the pancreas, and reveals adult pancreatic duct cells as a latent multipotent cell type. We used microarray to compare adult mouse fbw7 knock out ductal cells with bonafide beta cells In order to isolate fbw7 ko, fbw7 wt ductal cells and beta cells we used adult mice with the following genotypes: MIP-GFP (beta cells are constitutively labelled with GFP), Ck19-CreERT; R26-LSL-YFP; Fbw7 +/+ (ductal cells are labelled with YFP upon tamoxifen injection) and Ck19-CreERT; R26-LSL-YFP; Fbw7 F/F mice (ductal cells are labelled with YFP upon tamoxifen injection). 30000 GFP+ cells were isolated by FACS-sorting. RNA was extracted and amplified using NuGEN kit.

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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo.

Project description:The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo.

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CHD4 remodels cellular chromatin accessibility and activates c-Myc pathway

Project description:To investigate whether there is a physiological interaction between CHD4 and c-Myc, we conducted MS and found that CHD4 interacted with c-Myc.

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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [ATAC-seq]

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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [RNA-seq]

Project description:The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [RNA-seq]

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Chromodomain Helicase DNA-binding 4 (CHD4) is required for B cell identity and lineage progression

Project description:B cell specification and identity are controlled by transcription factors and cytokine receptors that drive the expression of stage-specific transcriptomes during lineage progression. A key feature of these mechanisms is the repression of inappropriate transcription. Here, we utilized RNA-seq to demonstrate that chromodomain helicase DNA-binding protein 4 (CHD4), an ATPase/helicase subunit of Mi-2/NuRD chromatin remodeling complexes, is essential for B cell identity. In mice that lack CHD4 selectively in the B lineage, defects include developmental arrest at the early pro-B cell stage. While many pro-B-specific genes are expressed in the mutant cells, transcripts that are normally restricted to other tissues including pancreas and bone are expressed out of context. Moreover, CHD4-deficient pro-B cells do not proliferate in response to IL-7, exhibit greatly decreased utilization of distal VH segments and accumulate DNA damage. Together, our data confirm the importance of CHD4 and NuRD complexes for the generation of functional B cells.

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