ArticleMolecular oncology2014
Whole genome RNAi screens reveal a critical role of REV3 in coping with replication stress.
Article in Molecular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Inhibition of LDHB triggers DNA damage and increases cisplatin sensitivity in pleural mesothelioma.Oncogenesis · 2025Article
- MAD2L2 promotes replication fork protection and recovery in a shieldin-independent and REV3L-dependent manner.Nature communications · 2022Article
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- DNA polymerase ζ in DNA replication and repair.Nucleic acids research · 2019Review
- Rscreenorm: normalization of CRISPR and siRNA screen data for more reproducible hit selection.BMC bioinformatics · 2018Article
- DNA polymerase ζ deficiency causes impaired wound healing and stress-induced skin pigmentation.Life science alliance · 2018Article
- Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?PLoS genetics · 2017Review
- A flow cytometry-based method to simplify the analysis and quantification of protein association to chromatin in mammalian cells.Nature protocols · 2015Article
- Article
- Whole genome RNAi screens reveal a critical role of REV3 in coping with replication stress.Molecular oncology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
REV3, the catalytic subunit of translesion polymerase zeta (polζ), is commonly associated with DNA damage bypass and repair. Despite sharing accessory subunits with replicative polymerase δ, very little is known about the role of polζ in DNA replication. We previously demonstrated that inhibition of REV3 expression induces persistent DNA damage and growth arrest in cancer cells. To reveal determinants of this sensitivity and obtain insights into the cellular function of REV3, we performed whole human genome RNAi library screens aimed at identification of synthetic lethal interactions with REV3 in A549 lung cancer cells. The top confirmed hit was RRM1, the large subunit of ribonucleotide reductase (RNR), a critical enzyme of de novo nucleotide synthesis. Treatment with the RNR-inhibitor hydroxyurea (HU) synergistically increased the fraction of REV3-deficient cells containing single stranded DNA (ssDNA) as indicated by an increase in replication protein A (RPA). However, this increase was not accompanied by accumulation of the DNA damage marker γH2AX suggesting a role of REV3 in counteracting HU-induced replication stress (RS). Consistent with a role of REV3 in DNA replication, increased RPA staining was confined to HU-treated S-phase cells. Additionally, we found genes related to RS to be significantly enriched among the top hits of the synthetic sickness/lethality (SSL) screen further corroborating the importance of REV3 for DNA replication under conditions of RS.
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