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Related Experiment Video

Updated: Jan 16, 2026

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase

Published on: April 29, 2010

CFAP20 salvages arrested RNAPII from the path of co-directional replisomes.

Sidrit Uruci¹, Daphne E C Boer¹, Paul W Chrystal²

¹Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.

|January 14, 2026

Summary

This summary is machine-generated.

We discovered CFAP20 rescues arrested RNA polymerase II (RNAPII) near promoters, preventing replication conflicts. CFAP20 deficiency causes R-loops, replication defects, and genome instability.

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Last Updated: Jan 16, 2026

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase

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Published on: April 29, 2010

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CAPRRESI: Chimera Assembly by Plasmid Recovery and Restriction Enzyme Site Insertion

CAPRRESI: Chimera Assembly by Plasmid Recovery and Restriction Enzyme Site Insertion

Published on: June 25, 2017

Area of Science:

Molecular Biology
Genetics
Cell Biology

Background:

DNA replication and transcription must be coordinated to prevent machinery collisions, especially near promoters.
Arrested RNA polymerase II (RNAPII) at promoters can form R-loops and impede DNA replication initiation.
Mechanisms rescuing arrested RNAPII and preventing conflicts with co-directional replisomes are not fully understood.

Purpose of the Study:

To identify factors involved in rescuing arrested RNAPII near promoters.
To understand how arrested transcription impacts DNA replication dynamics.
To elucidate the role of CFAP20 in preventing transcription-replication conflicts.

Main Methods:

Genome-wide approaches
Genetic screens
Analysis of R-loop accumulation
Replication timing and dynamics assays

Main Results:

CFAP20 was identified as a key component of a pathway salvaging arrested RNAPII.
CFAP20 deficiency leads to R-loop accumulation, altered replication timing, and accelerated replication fork speeds.
Accelerated replication forks in trans cause reduced origin activity and single-stranded DNA gaps.
Co-depletion of Mediator or removal of R-loop-engaged RNAPII restored normal replication.

Conclusions:

CFAP20 facilitates RNAPII elongation, preventing replisome collisions by mitigating transcription-dependent replication fork stalling.
Arrested transcription complexes near promoters can propagate genome-wide replication phenotypes.
CFAP20 is crucial for maintaining genome stability by resolving transcription-replication conflicts.