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Related Concept Videos

Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
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Nucleosome Remodeling02:54

Nucleosome Remodeling

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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
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Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...
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Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

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Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
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Methods of Nuclear Reprogramming01:24

Methods of Nuclear Reprogramming

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Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for...
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Histone Modification02:32

Histone Modification

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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
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Related Experiment Video

Updated: Sep 15, 2025

Efficient Differentiation of Pluripotent Stem Cells to NKX6-1+ Pancreatic Progenitors
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CHD4 and NKX2.2 Cooperate to Regulate Beta Cell Function by Repressing Non-Beta Cell Gene Programs.

Dylan K Sarbaugh1, Thais Gaia Oliveira1, Michelle A Guney1

  • 1Barbara Davis Center for Diabetes, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

Biorxiv : the Preprint Server for Biology
|July 16, 2025
PubMed
Summary
This summary is machine-generated.

Chromodomain helicase DNA-binding protein 4 (CHD4) is crucial for pancreatic beta cell function. Loss of CHD4 impairs beta cell maturation and function, leading to diabetes in mice.

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Differentiation of Human Pluripotent Stem Cells into Insulin-Producing Islet Clusters
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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Genetics

Background:

  • NKX2.2 is a key transcription factor for pancreatic islet beta (β) cell identity and function.
  • Cofactor proteins modulating NKX2.2 activity in β cells remain largely uncharacterized.
  • Chromodomain helicase DNA-binding protein 4 (CHD4) is a nucleosome remodeler involved in gene regulation across various cell types.

Purpose of the Study:

  • To identify NKX2.2 interacting partners in pancreatic β cells.
  • To investigate the roles of CHD4 in β cell maturation and function, both dependent and independent of NKX2.2.
  • To generate and analyze conditional knockout mice lacking Chd4 specifically in β cells (Chd4 βKO).

Main Methods:

  • Unbiased proteomics screen to identify NKX2.2 interacting proteins.
  • Generation of Chd4 βKO mice for conditional gene deletion in β cells.
  • Assessment of β cell morphology, function, glucose homeostasis, insulin secretion, and calcium signaling in Chd4 βKO mice.

Main Results:

  • Proteomics identified CHD4 as an NKX2.2 interacting partner.
  • Chd4 deletion in β cells led to impaired islet integrity, maturation, and function.
  • Chd4 βKO mice exhibited early-onset diabetes, characterized by disrupted glucose-stimulated insulin secretion and calcium signaling.
  • Downregulation of essential β cell regulatory genes was observed in Chd4-deficient β cells.

Conclusions:

  • CHD4 acts as an essential transcriptional cofactor for NKX2.2 in pancreatic β cells.
  • CHD4 is indispensable for the proper maturation and sustained function of pancreatic β cells.
  • Disruption of CHD4 function in β cells leads to a diabetic phenotype.