ArticleThe Journal of biological chemistry2014
A missense mutation in Rev7 disrupts formation of Polζ, impairing mouse development and repair of genotoxic agent-induced DNA lesions.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Probing hot spots of protein-protein interactions mediated by the safety-belt region of REV7.Structure (London, England : 1993) · 2024Article
- Primordial germ cell DNA demethylation and development require DNA translesion synthesis.Nature communications · 2024Article
- REV7: a small but mighty regulator of genome maintenance and cancer development.Frontiers in oncology · 2024Review
- Investigating the Functional Roles of Aldehyde Dehydrogenase 3A1 in Human Corneal Epithelial Cells.International journal of molecular sciences · 2023Article
- REV7 in Cancer Biology and Management.Cancers · 2023Review
- Large-scale analyses of the X chromosome in 2,354 infertile men discover recurrently affected genes associated with spermatogenic failure.American journal of human genetics · 2022Article
- REV7: Jack of many trades.Trends in cell biology · 2021Review
- Hybrid Sterility with Meiotic Metaphase Arrest in Intersubspecific Mouse Crosses.The Journal of heredity · 2019Article
- 53BP1 cooperation with the REV7-shieldin complex underpins DNA structure-specific NHEJ.Nature · 2018Article
- Development of reproductive engineering techniques at the RIKEN BioResource Center.Experimental animals · 2017Review
- Identification of the first small-molecule inhibitor of the REV7 DNA repair protein interaction.Bioorganic & medicinal chemistry · 2016Article
- Biallelic inactivation of REV7 is associated with Fanconi anemia.The Journal of clinical investigation · 2016Article
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- REV7 is essential for DNA damage tolerance via two REV3L binding sites in mammalian DNA polymerase ζ.Nucleic acids research · 2015Article
- Hypersensitivity of primordial germ cells to compromised replication-associated DNA repair involves ATM-p53-p21 signaling.PLoS genetics · 2014Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Repro22 is a mutant mouse produced via N-ethyl-N-nitrosourea-induced mutagenesis that shows sterility with germ cell depletion caused by defective proliferation of primordial germ cells, decreased body weight, and partial lethality during embryonic development. Using a positional cloning strategy, we identified a missense mutation in Rev7/Mad2l2 (Rev7(C70R)) and confirmed that the mutation is the cause of the defects in repro22 mice through transgenic rescue with normal Rev7. Rev7/Mad2l2 encodes a subunit of DNA polymerase ζ (Polζ), 1 of 10 translesion DNA synthesis polymerases known in mammals. The mutant REV7 did not interact with REV3, the catalytic subunit of Polζ. Rev7(C70R/C70R) cells showed decreased proliferation, increased apoptosis, and arrest in S phase with extensive γH2AX foci in nuclei that indicated accumulation of DNA damage after treatment with the genotoxic agent mitomycin C. The Rev7(C70R) mutation does not affect the mitotic spindle assembly checkpoint. These results demonstrated that Rev7 is essential in resolving the replication stalls caused by DNA damage during S phase. We concluded that Rev7 is required for primordial germ cell proliferation and embryonic viability and development through the translesion DNA synthesis activity of Polζ preserving DNA integrity during cell proliferation, which is required in highly proliferating embryonic cells.
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