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Updated: Aug 6, 2026

Artificial RNA Polymerase II Elongation Complexes for Dissecting Co-transcriptional RNA Processing Events
Published on: May 13, 2019
ATR activity regulates DNA replication and RNA polymerase II transcription during S-phase
Jianming Wang1, Sudipta Pathak1, Megan Jones1
1Department of Cancer and Genomic Sciences, School of Medical Sciences, College of Medicine and Health, University of Birmingham, Birmingham B15 2TT, UK.
Cells regulate transcription during DNA replication using ATR activity. This control prevents conflicts and may link to cancer phenotypes involving deregulated ATR.
Area of Science:
- Molecular Biology
- Genetics
- Cell Biology
Background:
- Transcription and DNA replication share the DNA template.
- Conflicts between these processes can lead to genome instability.
- Recent findings indicate temporal and spatial coexistence of transcription and replication.
Purpose of the Study:
- To identify mechanisms controlling transcription activity during S-phase.
- To investigate the role of ATR activity in regulating transcription during replication.
- To explore the link between transcription regulation during S-phase and cancer phenotypes.
Main Methods:
- Analysis of RNA polymerase II loading and progression.
- Assessment of gene transcription regulation during S-phase.
- Investigation of ATR pathway involvement.
- Correlation analysis with gene expression in cancer patients.
Main Results:
- Cells employ multiple mechanisms to control transcription during S-phase.
- Transcription regulation involves modulating RNA polymerase II loading and promoter-proximal pausing.
- These regulations are controlled by ATR activity.
- A correlation exists between affected genes and those with altered expression in ATR-deregulated cancers.
Conclusions:
- ATR plays a crucial role in managing transcription activity during S-phase.
- ATR-mediated transcription control during replication is a key mechanism for genome stability.
- Dysregulation of ATR's role in transcription during S-phase may contribute to cancer development.
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