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Chromatin reader Dido3 regulates the genetic network of B cell differentiation

ABSTRACT: Chromatin reader Dido3 regulates the genetic network of B cell differentiation

PROVIDER: PRJNA660474 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12558683_1.fastq.gz	Fastqsanger.gz
	SRR12558683_2.fastq.gz	Fastqsanger.gz
	SRR12558684_1.fastq.gz	Fastqsanger.gz
	SRR12558684_2.fastq.gz	Fastqsanger.gz
	SRR12558685_1.fastq.gz	Fastqsanger.gz

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Chromatin reader Dido3 regulates the genetic network of B cell differentiation

Project description:The development of hematopoietic lineages is based on a complex balance of transcription factors whose expression depends on the epigenetic signatures that characterize each differentiation step. The B cell lineage arises from hematopoietic stem cells through the stepwise silencing of stemness genes and balanced expression of mutually regulated transcription factors, as well as DNA rearrangement. Here we report the impact on B cell differentiation of lack of Dido3, a reader of the chromatin status, in the hematopoietic compartment. We found a reduced DNA accessibility in hematopoietic precursors, leading to severe deficiency in the generation of successive B cell differentiation stages. The expression of essential transcription factors and differentiation markers is affected, as is the somatic recombination process.

2022-09-29 | GSE157228 | GEO

The chromatin reader DIDO3 is a regulator of the gene network that controls B cell differentiation.

Project description:The chromatin reader DIDO3 is a regulator of the gene network that controls B cell differentiation.

| PRJNA1135225 | ENA

The chromatin reader DIDO3 is a regulator of the gene network that controls B cell differentiation.

Project description:The development of hematopoietic cell lineages is a highly complex process that is governed by a delicate interplay of various transcription factors. The expression of these factors is influenced, in part, by epigenetic signatures that define each stage of cell differentiation. In particular, the formation of B lymphocytes depends on the sequential silencing of stemness genes and the balanced expression of interdependent transcription factors, along with DNA rearrangement. We have investigated the impact that the deficiency of DIDO3, a protein involved in chromatin status readout, has on B cell differentiation within the hematopoietic compartment of mice. Our findings revealed significant impairments in the successive stages of B cell development. The absence of DIDO3 resulted in remarkable alterations in the expression of essential transcription factors and differentiation markers, which are crucial for orchestrating the differentiation process. In addition, the somatic recombination process, which is responsible for generation of antigen receptor diversity, was also adversely affected. These observations highlight the vital role of epigenetic regulation, in particular the involvement of DIDO3, in ensuring proper B cell differentiation. Further research into the mechanisms underlying these disruptive alterations will deepen our understanding of hematopoiesis and may potentially lead to insights that aid in the development of therapeutic interventions for disorders involving aberrant B cell development.

2025-04-30 | GSE272156 | GEO

Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (vsmutNT)

Project description:Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation. We used microarrays to determine how the deletion of exon 16 (C-terminal truncation) of the Dido3 affects gene expression that results in the suppression of ESC differentiation.

2017-03-16 | GSE85027 | GEO

Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (vsmutCT)

2017-03-16 | GSE85026 | GEO

Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (vsmut)

2017-03-16 | GSE85025 | GEO

Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (Affy)

2017-03-16 | GSE85006 | GEO

A LncRNA-MAF/MAFB transcription factor network regulates epidermal differentiation

Project description:A LncRNA-MAF/MAFB transcription factor network regulates epidermal differentiation

| PRJNA230531 | ENA

Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (ChIP-seq)

2017-03-16 | GSE85028 | GEO

Temporal Profiling of Epitranscriptomic Reader, Writer and Eraser Proteins during Osteogenic Differentiation of Human Embryonic Stem Cells

Project description:Osteogenesis is the process of bone formation and is modulated by multiple regulatory networks. With the rapid development of the epitranscriptomics field, RNA modifications and their reader, writer, and eraser (RWE) proteins are shown to be involved in the regulation of various biological processes. Few studies, however, were conducted to investigate the functions of RNA modifications and their RWE proteins in osteogenesis. By using a parallel-reaction monitoring (PRM)-based targeted proteomics method, we performed a comprehensive quantitative assessment of 154 epitranscriptomic RWE proteins during the time course of osteogenic differentiation of H9 human embryonic stem cells (ESCs). We found that approximately half of the 126 detected RWE proteins were downregulated during osteogenic differentiation, and they included mainly those proteins involved in RNA methylation and pseudouridine synthesis. Protein-protein interaction (PPI) network analysis revealed a high connectivity between the downregulated epitranscriptomic RWE proteins and osteogenesis-related proteins. Gene set enrichment analysis of previously published RNA-seq data from osteogenesis imperfecta patients suggested a potential role of METTL1, the top-ranked hub protein of downregulated RWE proteins, in osteogenesis through the cytokine network. Together, this is the first targeted profiling of epitranscriptomic RWE proteins during osteogenic differentiation of human ESCs and our work unveiled potential regulatory roles of these proteins in osteogenesis.

2023-05-23 | PXD039249 | Pride

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