Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Lineage Commitment01:21

Lineage Commitment

4.1K
Commitment is the  process whereby stem cells:
4.1K
Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

2.1K
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...
2.1K
Epigenetic Regulation01:37

Epigenetic Regulation

3.7K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
3.7K
Epigenetic Regulation01:46

Epigenetic Regulation

33.4K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
33.4K
Inheritance of Chromatin Structures03:17

Inheritance of Chromatin Structures

7.2K
Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
7.2K
Histone Modification02:32

Histone Modification

15.9K
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
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone...
15.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Multi-omic profiling of human antibody-secreting cells reveals diverse subsets sustain durable humoral immunity.

bioRxiv : the preprint server for biology·2026
Same author

Development and function of specified thymic iNKT1 cells critically depend on an Ets1-Tbet transcription factor axis.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same author

Chromatin interaction-based annotation of regulatory elements reveals dynamic promoter-enhancer interactions in lymphocyte development.

iScience·2025
Same author

Ontogeny shapes the ability of ETV6::RUNX1 to enhance hematopoietic stem cell self-renewal and disrupt early lymphopoiesis.

Leukemia·2024
Same author

Concurrent stem- and lineage-affiliated chromatin programs precede hematopoietic lineage restriction.

Cell reports·2023
Same author

TGF-β Promotes the Postselection Thymic Development and Peripheral Function of IFN-γ-Producing Invariant NKT cells.

Journal of immunology (Baltimore, Md. : 1950)·2023
Same journal

Corrigendum: Inhibition of Myc family proteins eradicates KRas-driven lung cancer in mice.

Genes & development·2026
Same journal

A new perspective on ATR's role in translesion synthesis.

Genes & development·2026
Same journal

Mechanisms coordinating exit from the stem cell state in mammals.

Genes & development·2026
Same journal

Evolutionarily conserved spliceosome-exosome pathway in nuclear mRNA surveillance.

Genes & development·2026
Same journal

CDK1 and CEP97 cooperatively control centriole length to orchestrate ciliogenesis and developmental patterning.

Genes & development·2026
Same journal

Coupling of translesion synthesis with the replisome stabilized at stalled replication forks by ATR.

Genes & development·2026
See all related articles

Related Experiment Video

Updated: Jan 10, 2026

Direct Lineage Reprogramming of Adult Mouse Fibroblast to Erythroid Progenitors
11:46

Direct Lineage Reprogramming of Adult Mouse Fibroblast to Erythroid Progenitors

Published on: December 14, 2018

6.8K

B-lineage commitment is dependent on a reversible epigenetic switch.

Johanna Tingvall-Gustafsson1,2, Kim Hellerstedt1, Jonas Ungerbäck2

  • 1Department of Biomedical and Clinical Sciences, Linköping University, 58185 Linköping, Sweden.

Genes & Development
|November 20, 2025
PubMed
Summary
This summary is machine-generated.

Early B-cell development involves an epigenetic switch, driven by transcription factors, that silences T-cell genes. This process ensures B-lymphoid commitment by suppressing inherent T-lineage potential.

Keywords:
B-lymphocytesepigeneticstranscription

More Related Videos

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
10:28

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

Published on: September 20, 2018

6.8K
Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation
11:06

Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation

Published on: September 20, 2017

6.5K

Related Experiment Videos

Last Updated: Jan 10, 2026

Direct Lineage Reprogramming of Adult Mouse Fibroblast to Erythroid Progenitors
11:46

Direct Lineage Reprogramming of Adult Mouse Fibroblast to Erythroid Progenitors

Published on: December 14, 2018

6.8K
Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
10:28

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

Published on: September 20, 2018

6.8K
Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation
11:06

Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation

Published on: September 20, 2017

6.5K

Area of Science:

  • Immunology
  • Developmental Biology
  • Epigenetics

Background:

  • Understanding B-lymphoid development requires insight into transcription factor networks and epigenetic regulation.
  • Early lymphoid progenitors possess potential for multiple lineages, including T-cells.

Purpose of the Study:

  • To model early B-cell development using high-resolution DNA accessibility data.
  • To investigate the interplay between transcription factors and the epigenome during B-lymphoid commitment.

Main Methods:

  • Combined single-cell RNA sequencing (SC-RNA) and ATAC sequencing (SC-ATAC) on bone marrow progenitor populations.
  • Trend change analysis to identify shifts in DNA accessibility during development.

Main Results:

  • A high-resolution model of B-cell development was established based on DNA accessibility changes.
  • A rapid epigenetic switch was identified, leading to loss of T-lineage priming and acquisition of B-lymphocyte epigenome.
  • This switch correlated with the activation of key B-lineage transcription factors (Ebf1, Pax5).

Conclusions:

  • B-lymphoid commitment is mediated by a transcription factor-driven, dose-dependent epigenetic switch.
  • Epigenetic silencing is crucial for maintaining B-cell fate, as demonstrated by EZH1/EZH2 inhibition studies.
  • This switch suppresses the inherent T-lineage potential in early lymphoid progenitors.