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

Chromatin Position Affects Gene Expression02:35

Chromatin Position Affects Gene Expression

25.2K
Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
Topologically Associated Domains (TADs)
The 3-dimensional positioning of chromatin in the nucleus influences the...
25.2K
Chromatin Structure Regulates pre-mRNA Processing02:41

Chromatin Structure Regulates pre-mRNA Processing

8.4K
In eukaryotic cells, nascent mRNA transcripts need to undergo many post-transcriptional modifications to reach the cell cytoplasm and translate into functional proteins. For a long time, transcription and pre-mRNA processing were considered two independent events that occur sequentially in the cell. However, it has now been well established that transcription and pre-mRNA processing are two simultaneous processes that are precisely regulated inside the cell.
The chromatin structure, especially...
8.4K
Histone Modification02:32

Histone Modification

17.1K
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...
17.1K
Inheritance of Chromatin Structures03:17

Inheritance of Chromatin Structures

7.8K
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...
7.8K
Duplication of Chromatin Structure02:05

Duplication of Chromatin Structure

7.6K
The process of chromosome duplication during cell division requires genome-wide disruption and re-assembly of chromatin. The chromatin structure must be accurately inherited, reassembled, and maintained in the daughter cells to ensure lineage propagation.
The basic unit of the chromatin is the nucleosome, consisting of DNA wrapped around octameric histone proteins and short stretches of linker DNA separating individual nucleosomes. The histone proteins within the nucleosome have their...
7.6K
Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

9.9K
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...
9.9K

You might also read

Related Articles

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

Sort by
Same author

ASF1B promotes erythropoiesis by regulating the establishment and enrichment of H3.3 nucleosomes.

Nucleic acids research·2026
Same author

Mutations of six amino acid residues in a B domain-deleted blood coagulation factor VIII have a cumulative effect on increasing its secretion.

Research and practice in thrombosis and haemostasis·2026
Same author

LDB1 regulates gene expression and chromatin structure in pluripotency and lineage differentiation.

Nucleic acids research·2026
Same author

Chromatin-Associated RNAs Regulate Gene Expression and Chromatin Structure.

Non-coding RNA·2025
Same author

RNA-binding proteins pull in chromatin loops.

Nature cell biology·2025
Same author

LDB1 regulates gene expression and chromatin structure in pluripotency and lineage differentiation.

bioRxiv : the preprint server for biology·2025

Related Experiment Video

Updated: Mar 25, 2026

CRISPR-Mediated Reorganization of Chromatin Loop Structure
09:20

CRISPR-Mediated Reorganization of Chromatin Loop Structure

Published on: September 14, 2018

13.2K

Chromatin looping as a target for altering erythroid gene expression.

Ivan Krivega1, Ann Dean1

  • 1Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland.

Annals of the New York Academy of Sciences
|February 27, 2016
PubMed
Summary

Altering chromosome looping can activate fetal globin gene expression and reduce adult beta-globin gene expression. This chromosome folding mechanism offers a potential therapeutic target for beta-hemoglobinopathies like sickle cell disease and thalassemia.

Keywords:
chromatin loopingenhancerfetal hemoglobinglobin switchingthalassemia

More Related Videos

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

7.0K
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

7.0K

Related Experiment Videos

Last Updated: Mar 25, 2026

CRISPR-Mediated Reorganization of Chromatin Loop Structure
09:20

CRISPR-Mediated Reorganization of Chromatin Loop Structure

Published on: September 14, 2018

13.2K
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

7.0K
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

7.0K

Area of Science:

  • Genetics
  • Molecular Biology
  • Epigenetics

Background:

  • Beta-hemoglobinopathies are common single-gene disorders manifesting after fetal gamma-globin gene silencing and adult beta-globin gene activation.
  • Genome organization and chromosome folding are critical regulators of gene transcription.
  • Transcriptional enhancers drive gene expression over long distances by physically contacting target promoters via chromosome looping.

Purpose of the Study:

  • To investigate if redirecting enhancer activity through chromosome folding can alter gene transcription.
  • To explore the therapeutic potential of targeting chromosome looping for beta-hemoglobinopathies.

Main Methods:

  • Targeting the beta-globin locus control region (LCR) to the gamma-globin gene in adult erythroid cells via tethering.
  • Epigenetic unmasking of silenced gamma-globin genes.
  • Assessing the frequency of LCR/gamma-globin and LCR/beta-globin contacts.
  • Measuring gamma-globin and beta-globin transcription levels.

Main Results:

  • Redirecting the LCR to the gamma-globin gene increased LCR/gamma-globin contacts and decreased LCR/beta-globin contacts.
  • These manipulations resulted in robust, pancellular activation of gamma-globin transcription.
  • Concomitant reduction in beta-globin transcription was observed.

Conclusions:

  • Chromosome looping is a key mechanism regulating globin gene switching.
  • Modulating chromosome looping can be a viable therapeutic strategy for activating fetal hemoglobin in beta-thalassemia and sickle cell disease.