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Related Concept Videos

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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Nuclear reprogramming is the process of switching gene expression of one cell type to that of another cell type, usually from a differentiated cell state to an undifferentiated cell state. Differentiation occurs during processes such as development and morphogenesis, tissue regeneration, and malignancy. Cells can also be artificially induced to reprogram their gene expression by techniques such as nuclear transfer, induced pluripotency, and cell fusion. Such techniques have many applications in...
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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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Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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Groups of proteins may form a complex where each protein in this complex has a different role in the overall execution of the complex’s function. Often some of the proteins in the complex can be replaced by a closely related variant to give a complex that contains many of the same components yet is functionally distinct.
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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.
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Related Experiment Video

Updated: Jul 29, 2025

Application of RNAi and Heat-shock-induced Transcription Factor Expression to Reprogram Germ Cells to Neurons in C. elegans
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The NuRD complex cooperates with SALL4 to orchestrate reprogramming.

Bo Wang1,2,3,4, Chen Li3,5,6, Jin Ming1,3,5,6

  • 1Laboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.

Nature Communications
|May 19, 2023
PubMed
Summary
This summary is machine-generated.

The NuRD complex and Sall4 protein collaborate to close open chromatin during somatic cell reprogramming. This Sall4-NuRD interaction is crucial for efficient cell fate changes and iPSC generation.

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Area of Science:

  • Epigenetics and Gene Regulation
  • Stem Cell Biology
  • Chromatin Dynamics

Background:

  • Cell fate decisions involve complex genomic alterations.
  • Chromatin structure plays a critical role in regulating gene expression during cell reprogramming.
  • The precise mechanisms of chromatin remodeling in somatic cell reprogramming are not fully understood.

Purpose of the Study:

  • To investigate the role of the Nucleosome Remodeling Deacetylase (NuRD) complex in somatic cell reprogramming.
  • To elucidate the interaction between Sall4 and the NuRD complex during the early stages of reprogramming.
  • To understand how chromatin accessibility is modulated during cell fate transitions.

Main Methods:

  • Utilized mouse embryonic fibroblasts (MEFs) for induced pluripotent stem cell (iPSC) generation.
  • Investigated the recruitment of NuRD components by Sall4.
  • Employed genetic manipulation (knocking down NuRD components, mutating Sall4's NuRD-interacting motif).
  • Assessed reprogramming efficiency and chromatin accessibility dynamics.
  • Performed rescue experiments by grafting the NuRD-interacting motif onto Jdp2.

Main Results:

  • Sall4 is essential for recruiting endogenous NuRD components during reprogramming.
  • Disrupting the Sall4-NuRD interaction significantly impairs reprogramming efficiency.
  • Partial rescue of reprogramming defects was achieved by modifying Jdp2 to interact with NuRD.
  • The Sall4-NuRD axis is critical for closing open chromatin in early reprogramming.
  • Genes within Sall4-NuRD-closed chromatin loci are resistant to reprogramming.

Conclusions:

  • The NuRD complex plays a previously unrecognized role in somatic cell reprogramming.
  • The Sall4-NuRD interaction is a critical regulator of chromatin accessibility during cell fate decisions.
  • Chromatin closing is identified as a key step in controlling cell fate transitions.