Oxidative DNA damage bypass in Arabidopsis thaliana requires DNA polymerase λ and proliferating cell nuclear antigen 2
Autor: | Catherine Bergounioux, Giovanni Maga, Cécile Raynaud, Lorenzo Concia, Alessandra Amoroso, Caterina Maggio, Emmanuele Crespan, Rino Cella |
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Rok vydání: | 2011 |
Předmět: |
Guanine
DNA Plant DNA polymerase DNA repair DNA polymerase II Arabidopsis Plant Science DNA polymerase delta Proliferating Cell Nuclear Antigen Humans Cloning Molecular DNA Polymerase beta Research Articles biology Arabidopsis Proteins Protoplasts DNA replication Cell Biology Processivity Base excision repair Plants Genetically Modified Molecular biology Oxidative Stress biology.protein DNA polymerase mu DNA Damage |
Zdroj: | The Plant cell. 23(2) |
ISSN: | 1532-298X |
Popis: | The oxidized base 7,8-oxoguanine (8-oxo-G) is the most common DNA lesion generated by reactive oxygen species. This lesion is highly mutagenic due to the frequent misincorporation of A opposite 8-oxo-G during DNA replication. In mammalian cells, the DNA polymerase (pol) family X enzyme DNA pol λ catalyzes the correct incorporation of C opposite 8-oxo-G, together with the auxiliary factor proliferating cell nuclear antigen (PCNA). Here, we show that Arabidopsis thaliana DNA pol λ, the only member of the X family in plants, is as efficient in performing error-free translesion synthesis past 8-oxo-G as its mammalian homolog. Arabidopsis, in contrast with animal cells, possesses two genes for PCNA. Using in vitro and in vivo approaches, we observed that PCNA2, but not PCNA1, physically interacts with DNA pol λ, enhancing its fidelity and efficiency in translesion synthesis. The levels of DNA pol λ in transgenic plantlets characterized by overexpression or silencing of Arabidopsis POLL correlate with the ability of cell extracts to perform error-free translesion synthesis. The important role of DNA pol λ is corroborated by the observation that the promoter of POLL is activated by UV and that both overexpressing and silenced plants show altered growth phenotypes. |
Databáze: | OpenAIRE |
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