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

Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

6.2K
DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
6.2K
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

4.3K
At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
4.3K
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

3.3K
The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
3.3K

You might also read

Related Articles

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

Sort by
Same author

mRNA vaccines engage unconventional pathways in CD8<sup>+</sup> T cell priming.

Nature·2026
Same author

CD8<sup>+</sup> T cells are primed by cDC1 and exacerbate tau-mediated neurodegeneration.

bioRxiv : the preprint server for biology·2026
Same author

Transcription factor Maf promotes expression of repressor Zeb2 to drive microglia development in primitive hematopoiesis.

Immunity·2025
Same author

WDFY4-dependent cross-presentation proceeds via a vacuolar antigen-processing route.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

ID2 secures cDC1 specification by antagonizing E proteins at a pleiotropic <i>Zeb2</i> enhancer.

Research square·2025
Same author

Combined Flt3L and CD40 agonism restores dendritic cell-driven T cell immunity in pancreatic cancer.

Science immunology·2025

Related Experiment Video

Updated: Jan 10, 2026

Author Spotlight: Getting an A with the 3Cs: Chromosome Conformation Capture for Undergraduates
09:13

Author Spotlight: Getting an A with the 3Cs: Chromosome Conformation Capture for Undergraduates

Published on: May 12, 2023

4.3K

The Making of a cDC1: Precision Programming of Progenitor Potential.

Theresa L Murphy1, Kenneth M Murphy1

  • 1Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA.

Immunological Reviews
|November 27, 2025
PubMed
Summary
This summary is machine-generated.

The development of type 1 classical dendritic cells (cDC1s) relies on a precise network of gene enhancers. This study reveals a sequential, cis-dependent mechanism that progressively activates enhancers to ensure robust cDC1 lineage commitment.

Keywords:
BATF3C/EBPID2IRF8NFIL3dendritic cellsdevelopmenttranscription

More Related Videos

Efficient and Cost Effective Electroporation Method to Study Primary Cilium-Dependent Signaling Pathways in the Granule Cell Precursor
04:06

Efficient and Cost Effective Electroporation Method to Study Primary Cilium-Dependent Signaling Pathways in the Granule Cell Precursor

Published on: November 30, 2021

2.7K
Author Spotlight: Identifying Compensatory Pathways in Malaria Parasites Containing Hypomorphic Allele of Essential Protein Kinases
09:13

Author Spotlight: Identifying Compensatory Pathways in Malaria Parasites Containing Hypomorphic Allele of Essential Protein Kinases

Published on: November 22, 2024

1.8K

Related Experiment Videos

Last Updated: Jan 10, 2026

Author Spotlight: Getting an A with the 3Cs: Chromosome Conformation Capture for Undergraduates
09:13

Author Spotlight: Getting an A with the 3Cs: Chromosome Conformation Capture for Undergraduates

Published on: May 12, 2023

4.3K
Efficient and Cost Effective Electroporation Method to Study Primary Cilium-Dependent Signaling Pathways in the Granule Cell Precursor
04:06

Efficient and Cost Effective Electroporation Method to Study Primary Cilium-Dependent Signaling Pathways in the Granule Cell Precursor

Published on: November 30, 2021

2.7K
Author Spotlight: Identifying Compensatory Pathways in Malaria Parasites Containing Hypomorphic Allele of Essential Protein Kinases
09:13

Author Spotlight: Identifying Compensatory Pathways in Malaria Parasites Containing Hypomorphic Allele of Essential Protein Kinases

Published on: November 22, 2024

1.8K

Area of Science:

  • Immunology
  • Developmental Biology
  • Genomics

Background:

  • Type 1 classical dendritic cells (cDC1s) are crucial immune cells derived from bone marrow progenitors.
  • Their development is orchestrated by a complex transcriptional network centered on interferon regulatory factor-8 (IRF8).
  • Stage-specific expression of IRF8 is regulated by a super-enhancer and multiple upstream enhancers.

Purpose of the Study:

  • To elucidate the intricate transcriptional network governing cDC1 development.
  • To understand the role of specific enhancers and transcription factors in lineage commitment.
  • To investigate the cis-dependent mechanism regulating enhancer activation during cDC1 differentiation.

Main Methods:

  • Analysis of Irf8 enhancer activity during progenitor differentiation.
  • Investigation of transcription factor roles (IRF8, C/EBPα, E-proteins, NFIL3, ZEB2, ID2, BATF3, JUN).
  • Studies involving compound enhancer deletions to assess cis-dependency.

Main Results:

  • A sequential enhancer activation cascade (starting with C/EBPα at +56kb, E-proteins at +41kb, and NFIL3-driven switch to +32kb) controls IRF8 expression.
  • NFIL3-mediated suppression of ZEB2 is critical for de-repressing ID2 and BATF3, leading to cDC1 fate.
  • The +32kb enhancer utilizes suboptimized elements for BATF3 auto-regulation, crucial for cDC1/cDC2 divergence.
  • cis-dependent regulation ensures sequential enhancer function, progressively tuning chromatin accessibility for lineage commitment.
  • Disruption of NFIL3/ZEB2 balance or IL-6-induced C/EBPβ can abrogate cDC1 development.

Conclusions:

  • cDC1 development is governed by a sequential, cis-regulated enhancer cascade ensuring robust lineage commitment.
  • This mechanism provides a novel model for understanding developmental genomic regulation.
  • Understanding this pathway is critical for controlling immune cell differentiation and function.