An increase of oxidised nucleotides activates DNA damage checkpoint pathway that regulates post-embryonic development in Caenorhabditis elegans

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Názov: An increase of oxidised nucleotides activates DNA damage checkpoint pathway that regulates post-embryonic development in Caenorhabditis elegans
Autori: Sanada, Yu, Zhang-Akiyama, Qiu-Mei
Prispievatelia: 秋山, 秋梅
Zdroj: Mutagenesis. 29:107-114
Informácie o vydavateľovi: Oxford University Press (OUP), 2014.
Rok vydania: 2014
Predmety: Pyrophosphatases/metabolism, Paraquat, 0301 basic medicine, DNA Repair Enzymes/metabolism, Xeroderma Pigmentosum Group A Protein/metabolism, Pyrophosphatases/genetics, Telomere-Binding Proteins, Oxidative Stress/physiology, Nucleotides/metabolism, Caenorhabditis elegans/growth & development, Deoxyguanine Nucleotides/metabolism, Caenorhabditis elegans Proteins/genetics, 03 medical and health sciences, Escherichia coli, Animals, Pyrophosphatases, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Chromatography, High Pressure Liquid, DNA Primers, 2. Zero hunger, Chromatography, DNA Primers/genetics, Telomere-Binding Proteins/metabolism, DNA Damage/physiology, Signal Transduction/physiology, Nucleotides, Deoxyguanine Nucleotides, Vitamin K 3, Nucleotides/genetics, Phosphoric Monoester Hydrolases, 3. Good health, Checkpoint Kinase 2, Oxidative Stress, DNA Repair Enzymes, High Pressure Liquid, Gene Knockdown Techniques, Checkpoint Kinase 2/metabolism, RNA Interference, Caenorhabditis elegans Proteins/metabolism, Phosphoric Monoester Hydrolases/metabolism, DNA Damage, Signal Transduction
Popis: 8-Oxo-dGTP, an oxidised form of dGTP generated in the nucleotide pool, can be incorporated opposite adenine or cytosine in template DNA, which can in turn induce mutations. In this study, we identified a novel MutT homolog (NDX-2) of Caenorhabditis elegans that hydrolyzes 8-oxo-dGDP to 8-oxo-dGMP. In addition, we found that NDX-1, NDX-2 and NDX-4 proteins have 8-oxo-GTPase or 8-oxo-GDPase activity. The sensitivity of ndx-2 knockdown C. elegans worms to methyl viologen and menadione bisulphite was increased compared with that of control worms. This sensitivity was rescued by depletion of chk-2 and clk-2, suggesting that growth of the worms is regulated by the checkpoint pathway in response to the accumulation of oxidised nucleotides. Moreover, we found that the sensitivity to menadione bisulphite of ndx-1 and ndx-2-double knockdown worms was enhanced by elimination of XPA-1, a factor involved in nucleotide excision repair. The rescue effect by depletion of chk-2 and clk-2 was limited in the xpa-1 mutant, suggesting that the chk-2 and clk-2 checkpoint pathway is partially linked to the function of XPA-1.
Druh dokumentu: Article
Popis súboru: application/pdf
Jazyk: English
ISSN: 1464-3804
0267-8357
DOI: 10.1093/mutage/get067
Prístupová URL adresa: https://academic.oup.com/mutage/article-pdf/29/2/107/17162975/get067.pdf
https://pubmed.ncbi.nlm.nih.gov/24435662
https://ci.nii.ac.jp/naid/120005587838
https://academic.oup.com/mutage/article/29/2/107/1168559
https://repository.kulib.kyoto-u.ac.jp/dspace/handle/2433/196886
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3924892/
http://repository.kulib.kyoto-u.ac.jp/dspace/bitstream/2433/196886/1/mutage_get067.pdf
https://paperity.org/p/41649029/an-increase-of-oxidised-nucleotides-activates-dna-damage-checkpoint-pathway-that
Prístupové číslo: edsair.doi.dedup.....2bacdbc44932328ec99eced7f9eb1bf2
Databáza: OpenAIRE
Popis
Abstrakt:8-Oxo-dGTP, an oxidised form of dGTP generated in the nucleotide pool, can be incorporated opposite adenine or cytosine in template DNA, which can in turn induce mutations. In this study, we identified a novel MutT homolog (NDX-2) of Caenorhabditis elegans that hydrolyzes 8-oxo-dGDP to 8-oxo-dGMP. In addition, we found that NDX-1, NDX-2 and NDX-4 proteins have 8-oxo-GTPase or 8-oxo-GDPase activity. The sensitivity of ndx-2 knockdown C. elegans worms to methyl viologen and menadione bisulphite was increased compared with that of control worms. This sensitivity was rescued by depletion of chk-2 and clk-2, suggesting that growth of the worms is regulated by the checkpoint pathway in response to the accumulation of oxidised nucleotides. Moreover, we found that the sensitivity to menadione bisulphite of ndx-1 and ndx-2-double knockdown worms was enhanced by elimination of XPA-1, a factor involved in nucleotide excision repair. The rescue effect by depletion of chk-2 and clk-2 was limited in the xpa-1 mutant, suggesting that the chk-2 and clk-2 checkpoint pathway is partially linked to the function of XPA-1.
ISSN:14643804
02678357
DOI:10.1093/mutage/get067