ArticlePlant physiology2011
Role of AtPolζ, AtRev1, and AtPolη in UV light-induced mutagenesis in Arabidopsis.
Article in Plant physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed.
- The relationship between DNA damage and repair and the occurrence and development of disease.Frontiers in genetics · 2026Review
- Plant tolerance mechanisms to DNA-damaging UV stress.Journal of experimental botany · 2025Review
- TEB/POLQ plays dual roles in protecting Arabidopsis from NO-induced DNA damage.Nucleic acids research · 2022Article
- The Dark Side of UV-Induced DNA Lesion Repair.Genes · 2020Review
- Structural Aspects of DNA Repair and Recombination in Crop Improvement.Frontiers in genetics · 2020Review
- Plant DNA Polymerases.International journal of molecular sciences · 2019Review
- Translesion Synthesis in Plants: Ultraviolet Resistance and Beyond.Frontiers in plant science · 2019Review
- Deletion of TLS polymerases promotes homologous recombination in Arabidopsis.Plant signaling & behavior · 2018Article
- Article
- DNA damage and repair in plants - from models to crops.Frontiers in plant science · 2015Review
- Role of AtPolζ, AtRev1 and AtPolη in γ ray-induced mutagenesis.Plant signaling & behavior · 2011Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Translesion synthesis (TLS) is a DNA damage tolerance mechanism in which DNA lesions are bypassed by specific polymerases. To investigate the role of TLS activities in ultraviolet light-induced somatic mutations, we analyzed Arabidopsis (Arabidopsis thaliana) disruptants of AtREV3, AtREV1, and/or AtPOLH genes that encode TLS-type polymerases. The mutation frequency in rev3-1 or rev1-1 mutants decreased compared with that in the wild type, suggesting that AtPolζ and AtRev1 perform mutagenic bypass events, whereas the mutation frequency in the polh-1 mutant increased, suggesting that AtPolη performs nonmutagenic bypass events with respect to ultraviolet light-induced lesions. The rev3-1 rev1-1 double mutant showed almost the same mutation frequency as the rev1-1 single mutant. The increased mutation frequency found in polh-1 was completely suppressed in the rev3-1 polh-1 double mutant, indicating that AtPolζ is responsible for the increased mutations found in polh-1. In summary, these results suggest that AtPolζ and AtRev1 are involved in the same (error-prone) TLS pathway that is independent from the other (error-free) TLS pathway mediated by AtPolη.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.