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

5.8K
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,...
5.8K
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

11.4K
As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
11.4K
Telomeres and Telomerase02:41

Telomeres and Telomerase

23.3K
In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded...
23.3K
Translesion DNA Polymerases02:10

Translesion DNA Polymerases

9.9K
Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...
9.9K
Single-Strand DNA Binding Proteins01:03

Single-Strand DNA Binding Proteins

14.1K
For successful DNA replication, the unwinding of double-stranded DNA must be accompanied by stabilization and protection of the separated single strands of the DNA. This crucial task is performed by single-strand DNA-binding (SSB) proteins. They bind to the DNA in a sequence-independent manner, which means that the nitrogenous bases of the DNA need not be present in a specific order for binding of SSB proteins to it. The binding of SSB proteins straightens single-stranded DNA (ssDNA) and makes...
14.1K
LTR Retrotransposons03:08

LTR Retrotransposons

17.4K
LTR retrotransposons are class I transposable elements with long terminal repeats flanking an internal coding region. These elements are less abundant in mammals compared to other class I transposable elements. About 8 percent of human genomic DNA comprises LTR retrotransposons. Some of the common examples of LTR retrotransposons are Ty elements in yeast and Copia elements in Drosophila.
The internal coding region of LTR retrotransposons and their mechanism of transposition closely resembles a...
17.4K

You might also read

Related Articles

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

Sort by
Same author

Covalent inhibitors of human papillomavirus type 16 E6 protein restore p53 function and suppress growth of HPV-driven tumors in vivo.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Spatial transcriptomics identifies dysregulated programs across neural and non-neural tissues in spinal muscular atrophy.

bioRxiv : the preprint server for biology·2026
Same author

ZPR1 Is Dispensable for HPV R-Loop Resolution but Regulates Host R-Loop Dynamics.

Viruses·2025
Same author

E2 Tyrosine 102 Regulates MmuPV1 Pathogenesis In Vivo.

Pathogens (Basel, Switzerland)·2025
Same author

Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis.

bioRxiv : the preprint server for biology·2025
Same author

Characteristics and outcomes of pediatric cerebral venous sinus thrombosis: Insights from the pediatric health information system database.

Thrombosis research·2025

Related Experiment Video

Updated: Jun 19, 2025

A G-quadruplex DNA-affinity Approach for Purification of Enzymatically Active G4 Resolvase1
11:25

A G-quadruplex DNA-affinity Approach for Purification of Enzymatically Active G4 Resolvase1

Published on: March 18, 2017

9.6K

Senataxin mediates R-loop resolution on HPV episomes.

Leny Jose1, Keely Smith2, Anaiya Crowner2

  • 1Department of Dermatology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Journal of Virology
|July 24, 2024
PubMed
Summary

The RNA-DNA helicase senataxin (SETX) resolves R-loops in human papillomavirus (HPV) episomal cells, preventing DNA damage and genome integration. SETX is crucial for maintaining viral transcription and episomal genome stability.

Keywords:
E2HPVR-loopsenataxin

More Related Videos

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
09:20

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells

Published on: July 23, 2010

15.7K
Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter
06:59

Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter

Published on: March 31, 2022

2.4K

Related Experiment Videos

Last Updated: Jun 19, 2025

A G-quadruplex DNA-affinity Approach for Purification of Enzymatically Active G4 Resolvase1
11:25

A G-quadruplex DNA-affinity Approach for Purification of Enzymatically Active G4 Resolvase1

Published on: March 18, 2017

9.6K
In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
09:20

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells

Published on: July 23, 2010

15.7K
Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter
06:59

Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter

Published on: March 31, 2022

2.4K

Area of Science:

  • Molecular Biology
  • Virology
  • Genetics

Background:

  • R-loops, three-stranded DNA-RNA structures, form during papillomavirus transcription.
  • These R-loops can impede transcription and replication, leading to DNA damage.
  • The mechanisms resolving R-loops in papillomavirus genomes were previously unknown.

Purpose of the Study:

  • To investigate the role of RNA-DNA helicases in resolving R-loops during human papillomavirus (HPV) transcription.
  • To determine the function of senataxin (SETX) in HPV episomal cell transcription and genome stability.

Main Methods:

  • Depletion of senataxin (SETX) using siRNAs in HPV-31 (CIN612) and HPV-16 (W12) episomal cell lines.
  • Analysis of R-loop accumulation at the viral early promoter via qPCR.
  • Assessment of viral transcript levels and genome integration rates.

Main Results:

  • SETX depletion significantly increased R-loop accumulation at the HPV early promoter.
  • Reduced viral transcripts were observed in SETX-depleted episomal HPV cell lines.
  • SETX depletion led to a notable increase in HPV genome integration.

Conclusions:

  • Senataxin (SETX) actively resolves R-loops at the HPV early promoter, facilitating transcription.
  • SETX plays a critical role in maintaining the episomal state of the HPV genome by preventing integration.
  • The interaction between SETX and the viral E2 protein is important for regulating HPV transcription and genome stability.