Who's on first in the cellular response to DNA damage?

Cline, Susan D.; Hanawalt, Philip C.

doi:10.1038/nrm1101

Cited by 123 publications

(85 citation statements)

References 140 publications

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“…The list of the genes involved in DNA repair activity [12,21,22], with their level of expression is listed in Table 1.…”

Section: Resultsmentioning

confidence: 99%

“…We also found a very high level of expression for H2AFX (H2A histone family member X) and CHAF1 (chromatin assembly factor 1), both involved in chromatin structure regulation during and after DNA repair. It must be pointed out that several types of regulation, in particular polyadenylation [17][18][19][20][21][22][23][24][25][26][27], will allow these mRNAs to be translated: portions of the mRNA can be lost both pre and post translation. Poly(A) binding proteins and the cytoplasmic polyadenylation elements are highly expressed in the oocyte (up to 500 times the background level).…”

Section: Discussionmentioning

confidence: 99%

“…The expression was classified as medium for a signal between 200 and 1,000; it was considered as high for a signal repeatedly over 1,000. Our references for the human DNA repair genes were based on Wood et al [12,21] and Cline and Hanawalt [22].…”

Section: Methodsmentioning

confidence: 99%

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Expression profile of genes coding for DNA repair in human oocytes using pangenomic microarrays, with a special focus on ROS linked decays

Ménézo

Russo

Tosti

et al. 2007

J Assist Reprod Genet

117

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Purpose To determine the level of expression for mRNAs that regulate DNA repair activity in oocytes at the germinal vesicle (GV) stage. Reactive oxygen species (ROS) have been shown to play a major role in the appearance of deleterious DNA decays, and this study focuses on the repair of damage linked to decay caused by the action of ROS. The oocyte needs a mechanism for repairing DNA decays in the early preimplantation embryo before the onset of genomic activation, since in the absence of repair, residual DNA damage would lead to either apoptosis or tolerance. Tolerance of DNA damage is a source of potential mutations. Method GV oocytes were selected for this study, both for the ethical reason that they are unsuitable for patient treatment, and because no transcription takes place during the period from GV to MII and then prior to genomic activation. The GV oocyte is therefore a good model for looking at DNA during the first cleavages of early preimplantation development. Six cohorts of GV oocytes were pooled for extraction of mRNA; the DNA was analysed using Affimetrix HG-UG133 Plus 2, containing 54,675 probe sets; spike and housekeeping genes were also added as internal controls. Results In GV oocytes, DNA repair pathways for oxidized bases are redundant. One step repair procedure (OSR), BER (base excision repair), MMR (mismatch repair) and NER (Nucleotide excision repair) are present. All the recognition proteins are also present. The chromatin assembly factors necessary for the maintenance of genomic stability are highly expressed. Conclusion Gene expression analysis shows that the oocyte does not allow a high level of tolerance for DNA decays. This regulatory mechanism should avoid transmitting mutations into the next generation.

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“…The list of the genes involved in DNA repair activity [12,21,22], with their level of expression is listed in Table 1.…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Expression profile of genes coding for DNA repair in human oocytes using pangenomic microarrays, with a special focus on ROS linked decays

Ménézo

Russo

Tosti

et al. 2007

J Assist Reprod Genet

117

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“…The mammalian DNA damage response comprises several features: sensing the damage, triggering signal transduction cascades, activating checkpoints to slow down or arrest cell cycle progression, changing chromatin structure at the site of the damage, and altering gene expression patterns in the cell. 1 The newly implemented gene expression profiles will, in turn, dictate whether the cell will undergo transient or terminal growth inhibition, increase proliferation, enter senescence or trigger cell death. Intriguingly however, the presence of damaged DNA causes an inhibition of general transcription through mechanisms that include the hyperphosphorylation of RNA polymerase II, the diverting of transcription factor (TF)IIH away from transcription and into repair, and the sequestration of TATA-binding protein (TBP) onto damaged DNA (reviewed in ref.…”

Section: Hur In the Mammalian Genotoxic Responsementioning

confidence: 99%

HuR in the Mammalian Genotoxic Response: Post-Transcriptional Multitasking

2003

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“…Among the repair mechanisms that cells use to cope with the genotoxic insults, nucleotide excision repair (NER) represents the most versatile and flexible DNA repair pathway in cells as it deals with a wide range of structurally unrelated bulky DNA lesions (5). In the mechanism of NER pathway, xeroderma pigmentosum group A (XPA) plays an indispensable role and is required for both global genome repair and transcription-coupled repair (6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Phosphorylation of Nucleotide Excision Repair Factor Xeroderma Pigmentosum Group A by Ataxia Telangiectasia Mutated and Rad3-Related–Dependent Checkpoint Pathway Promotes Cell Survival in Response to UV Irradiation

Shell

Yang

et al. 2006

Cancer Research

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DNA damage triggers complex cellular responses in eukaryotic cells, including initiation of DNA repair and activation of cell cycle checkpoints. In addition to inducing cell cycle arrest, checkpoint also has been suggested to modulate a variety of other cellular processes in response to DNA damage. In this study, we present evidence showing that the cellular function of xeroderma pigmentosum group A (XPA), a major nucleotide excision repair (NER) factor, could be modulated by checkpoint kinase ataxia-telangiectasia mutated and Rad3-related (ATR) in response to UV irradiation. We observed the apparent interaction and colocalization of XPA with ATR in response to UV irradiation. We showed that XPA was a substrate for in vitro phosphorylation by phosphatidylinositol-3-kinase-related kinase family kinases whereas in cells XPA was phosphorylated in an ATR-dependent manner and stimulated by UV irradiation. The Ser196 of XPA was identified as a biologically significant residue to be phosphorylated in vivo. The XPA-deficient cells complemented with XPA-S196A mutant, in which Ser196 was substituted with an alanine, displayed significantly higher UV sensitivity compared with the XPA cells complemented with wild-type XPA. Moreover, substitution of Ser196 with aspartic acid for mimicking the phosphorylation of XPA increased the cell survival to UV irradiation. Taken together, our results revealed a potential physical and functional link between NER and the ATRdependent checkpoint pathway in human cells and suggested that the ATR checkpoint pathway could modulate the cellular activity of NER through phosphorylation

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Who's on first in the cellular response to DNA damage?

Cited by 123 publications

References 140 publications

Expression profile of genes coding for DNA repair in human oocytes using pangenomic microarrays, with a special focus on ROS linked decays

Expression profile of genes coding for DNA repair in human oocytes using pangenomic microarrays, with a special focus on ROS linked decays

HuR in the Mammalian Genotoxic Response: Post-Transcriptional Multitasking

Phosphorylation of Nucleotide Excision Repair Factor Xeroderma Pigmentosum Group A by Ataxia Telangiectasia Mutated and Rad3-Related–Dependent Checkpoint Pathway Promotes Cell Survival in Response to UV Irradiation

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