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Published on: June 26, 2020
Mechanisms of Post-Replication DNA Repair
Yanzhe Gao1, Elizabeth Mutter-Rottmayer2,3, Anastasia Zlatanou4
1Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. yanzhe_gao@med.unc.edu.
Cells use post-replication repair (PRR) pathways, including trans-lesion synthesis (TLS) and template switching (TS), to maintain genome stability during DNA replication. These mechanisms tolerate or avoid DNA damage, preventing replication fork collapse and ensuring cell survival.
Area of Science:
- Molecular Biology
- Genetics
- Cell Biology
Background:
- Accurate DNA replication is vital for cell survival and genome stability.
- Cells encounter genotoxic injuries from internal and external sources.
- Post-replication repair (PRR) mechanisms tolerate DNA replication lesions, preventing fork collapse and double-strand breaks.
Purpose of the Study:
- To review current knowledge on PRR pathways.
- To discuss the primary mediators of PRR.
- To explain the regulation of PRR pathways within the DNA damage response.
Main Methods:
- Literature review of PRR mechanisms.
- Analysis of trans-lesion synthesis (TLS) and template switching (TS) pathways.
- Examination of signaling cascades integrating DNA synthesis and damage response.
Main Results:
- Two predominant PRR pathways exist: TLS and TS.
- TLS is a low-fidelity synthesis using specialized polymerases.
- TS is an error-free pathway using sister chromatids as templates.
Conclusions:
- Both TLS and TS are tightly regulated signaling cascades.
- PRR pathways are crucial for genome stability.
- Understanding PRR mediators and regulation is key to DNA damage response.
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