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USP7 is essential for maintaining Rad18 stability and DNA damage tolerance.

A Zlatanou1, S Sabbioneda2, E S Miller1

  • 1School of Cancer Sciences, University of Birmingham, Vincent Drive, Edgbaston, Birmingham, UK.

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|May 12, 2015
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Summary

The de-ubiquitylating enzyme USP7 stabilizes Rad18 protein levels, crucial for DNA damage tolerance and genome stability. Loss of USP7 impairs DNA repair pathways, impacting replication fidelity.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Rad18 is a key regulator of DNA damage response (DDR) pathways, balancing replication fidelity and genome stability.
  • Rad18 facilitates translesion synthesis (TLS) for damaged genome replication but can be error-prone.
  • Loss of Rad18 leads to replication fork collapse and incomplete genome replication.

Purpose of the Study:

  • To identify regulators of Rad18 protein levels.
  • To investigate the role of USP7 in the DNA damage response pathway involving Rad18.
  • To understand how USP7 impacts genome stability.

Main Methods:

  • Investigated the interaction between USP7 and Rad18.
  • Assessed the effect of USP7 depletion on Rad18 protein levels.
  • Analyzed UV-induced PCNA mono-ubiquitylation and Pol η recruitment.
  • Examined nascent DNA strand elongation and DNA damage tolerance in USP7-depleted cells.
  • Performed in vitro and in vivo experiments to study ubiquitin chain disassembly.

Main Results:

  • USP7 was identified as a critical regulator of Rad18 protein levels.
  • Loss of USP7 destabilizes Rad18, compromising UV-induced PCNA mono-ubiquitylation and Pol η recruitment.
  • USP7 depletion resulted in failed nascent daughter strand DNA elongation and reduced DNA damage tolerance.
  • USP7 directly associates with Rad18 and disassembles Rad18-dependent poly-ubiquitin chains.

Conclusions:

  • USP7 is a novel component of the cellular DNA damage response.
  • USP7 plays a crucial role in maintaining genome stability by regulating Rad18 levels and activity.
  • USP7-mediated regulation of Rad18 is essential for efficient DNA damage tolerance and replication fork protection.