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Updated: Nov 1, 2025

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
Published on: April 28, 2021
REV7 directs DNA repair pathway choice.
Connor S Clairmont1, Alan D D'Andrea2
1Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
REV7 protein is crucial for DNA repair, influencing choices between mutagenic and error-free pathways. Its HORMA domain and regulators like TRIP13 and p31 are key to DNA double-strand break (DSB) repair and Shieldin complex formation.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- REV7 protein is a key player in DNA repair pathways.
- Its role in translesion DNA synthesis is well-established, while its function in double-strand break (DSB) repair is a recent finding.
- REV7's HORMA domain is critical for its function.
Purpose of the Study:
- To review recent discoveries regarding REV7's function in DNA repair.
- To discuss the implications of REV7 in DNA repair pathway choice.
- To highlight the role of the HORMA domain and its regulators in DNA repair.
Main Methods:
- Literature review of recent studies on REV7.
- Analysis of REV7's involvement in translesion synthesis and DSB repair.
- Investigation of the Shieldin complex and HORMA domain regulators (TRIP13, p31).
Main Results:
- REV7's function in DSB repair has been recently discovered, leading to the identification of the Shieldin complex.
- The HORMA domain of REV7 is essential for its DNA repair functions.
- TRIP13 and p31 are identified as novel DNA repair factors regulating REV7.
Conclusions:
- REV7 acts as a critical determinant in choosing between mutagenic and error-free DNA repair pathways.
- The activation state of REV7's HORMA domain influences repair pathway selection at DSBs and replication forks.
- Recent findings expand our understanding of DNA repair mechanisms involving REV7 and the Shieldin complex.
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