Comparative Radiation Tolerance Based on the Induction of DNA Double-Strand Breaks in Tobacco BY-2 Cells and CHO-K1 Cells Irradiated with Gamma Rays

Yokota, Yuichiro; Shikazono, Naoya; Tanaka, Atsushi; Hase, Yoshihiro; Funayama, Tomoo; Wada, Seiichi; Inoue, Masayoshi

doi:10.1667/rr3355

Cited by 24 publications

(21 citation statements)

References 30 publications

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“…Dr. Kevin Culligan provided the atr and atr,atm segregating lines. We are extremely grateful to Dr. Steve Jacobsen and members of his lab for sharing histone preparation protocols and technical advice and to Dr. Y. Yokota for sharing in press data (Yokota et al, 2005). We thank Dr. Eli Hefner for ordering the ␥-H2AX peptide and antibody.…”

Section: Acknowledgmentsmentioning

confidence: 99%

“…Yokota et al performed PFGE (Rydberg et al, 1994;Lobrich et al, 1995;Whitaker et al, 1995) in tobacco BY-2 cells and Chinese hamster ovary (CHO) cells to directly quantitate and compare IR-dependent DSB induction. They determined DSB induction in tobacco cells was only onethird the rate of CHO cells (2.0 Ϯ 0.1 vs. 6.6 Ϯ 0.2 DSBs/ Gy-Gbp; Yokota et al, 2005), and the consistency of their CHO DSB induction data with previously published data suggests their methodology is reliable (Table 3; Cedervall et al, 1995). This suggests that plants are, like yeast and mammals, forming ␥-H2AX foci at DSBs and that the lower rate of focus formation observed in plants is simply due to a lower rate of damage induction by IR.…”

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confidence: 99%

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Ionizing Radiation–dependent γ-H2AX Focus Formation Requires Ataxia Telangiectasia Mutated and Ataxia Telangiectasia Mutated and Rad3-related

Friesner

Liu

Culligan

et al. 2005

MBoC

200

204

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The histone variant H2AX is rapidly phosphorylated at the sites of DNA double-strand breaks (DSBs). This phosphorylated H2AX (␥-H2AX) is involved in the retention of repair and signaling factor complexes at sites of DNA damage. The dependency of this phosphorylation on the various PI3K-related protein kinases (in mammals, ataxia telangiectasia mutated and Rad3-related [ATR], ataxia telangiectasia mutated [ATM], and DNA-PKCs) has been a subject of debate; it has been suggested that ATM is required for the induction of foci at DSBs, whereas ATR is involved in the recognition of stalled replication forks. In this study, using Arabidopsis as a model system, we investigated the ATR and ATM dependency of the formation of ␥ -H2AX foci in M-phase cells exposed to ionizing radiation (IR). We find that although the majority of these foci are ATM-dependent, ϳ10% of IR-induced ␥-H2AX foci require, instead, functional ATR. This indicates that even in the absence of DNA replication, a distinct subset of IR-induced damage is recognized by ATR. In addition, we find that in plants, ␥-H2AX foci are induced at only one-third the rate observed in yeasts and mammals. This result may partly account for the relatively high radioresistance of plants versus yeast and mammals. INTRODUCTIONThe induction of DNA double-strand breaks (DSBs) in eukaryotes triggers a number of protective responses including the upregulation of repair pathways, initiation of cell cycle arrest, and, in some organisms, the induction of programmed cell death. DSBs in actively dividing cells are particularly dangerous. Repair to form translocations and deletions can lead to loss of heterozygosity, which in turn leads to carcinogenesis in mammals or lethality in haploid yeast. For this reason all living things possess the ability to detect the presence of DSBs and relay this information to the cell cycle.Two important protein kinases involved in sensing and signaling DNA damage in eukaryotes are ataxia telangiectasia mutated (ATM) and ataxia telangiectasia mutated and rad3-related (ATR; Abraham, 2001;Sancar et al., 2004). In mammals, ATM is critical for responses to DSBs and signals downstream cell cycle checkpoint regulators including p53 and Chk2 to coordinate apoptotic responses and/or cell cycle arrest (Fernandez-Capetillo et al., 2002). In addition to checkpoint regulation, ATM responds to DSBs by interacting with proteins intimately involved in DNA repair such as the Mre11-Rad50-Nbs1 (M-R-N) complex (Gatei et al., 2000;van den Bosch et al., 2003) and RAD51 (Chen et al., 1999). In comparison, ATR, in a complex with the ATR interacting protein (ATRIP), is thought to respond primarily to agents that block replication, recognizing stalled replication forks and then signaling to Chk1 and p53 to induce cell cycle arrest, replication restart, and apoptosis (Abraham, 2001). In striking contrast to ATM, ATR is an essential gene in mammals; defects in the murine homolog cause early embryonic lethality and loss of ATR in conditional knock-out embryonic stem cells rapidly...

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Section: Acknowledgmentsmentioning

confidence: 99%

mentioning

confidence: 99%

Ionizing Radiation–dependent γ-H2AX Focus Formation Requires Ataxia Telangiectasia Mutated and Ataxia Telangiectasia Mutated and Rad3-related

Friesner

Liu

Culligan

et al. 2005

MBoC

200

204

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“…For instance, a comparative study of tobacco BY‐2 and Chinese hamster ovary cells showed that plant cells yielded one‐third less double‐strand breaks after the same dose of ionizing radiation (IR). Furthermore, the plant cells also tolerated a much higher number of DSBs before they died (Yokota et al , 2005). Despite the apparent power and their relevance for agriculture under changing environmental conditions, the plant DNA repair pathways are not very well understood.…”

Section: Introductionmentioning

confidence: 99%

The plant‐specific CDKB 1‐ CYCB 1 complex mediates homologous recombination repair in Arabidopsis

et al. 2016

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Upon DNA damage, cyclin‐dependent kinases (CDKs) are typically inhibited to block cell division. In many organisms, however, it has been found that CDK activity is required for DNA repair, especially for homology‐dependent repair (HR), resulting in the conundrum how mitotic arrest and repair can be reconciled. Here, we show that Arabidopsis thaliana solves this dilemma by a division of labor strategy. We identify the plant‐specific B1‐type CDKs (CDKB1s) and the class of B1‐type cyclins (CYCB1s) as major regulators of HR in plants. We find that RADIATION SENSITIVE 51 (RAD51), a core mediator of HR, is a substrate of CDKB1‐CYCB1 complexes. Conversely, mutants in CDKB1 and CYCB1 fail to recruit RAD51 to damaged DNA. CYCB1;1 is specifically activated after DNA damage and we show that this activation is directly controlled by SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1), a transcription factor that acts similarly to p53 in animals. Thus, while the major mitotic cell‐cycle activity is blocked after DNA damage, CDKB1‐CYCB1 complexes are specifically activated to mediate HR.

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“…The reason for these similarities and differences in the biological action of radiation on plant and animal objects remains unclear, but presumably is associated with DNA repair effectiveness [4].…”

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confidence: 99%

The Transcriptional Response of Arabidopsis thaliana L. Genes AtKu70, AtRAD51 and AtRad1 to X-Ray Radiation

Litvinov¹,

Rashydov²

2017

JAST-A

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Abstract:The study of influence of the fractionated and acute ionizing radiation on plants revealed that it is able to induce genomic instability. The hypothesis that transcription rate of several evolutionary conserved DNA repair genes AtKu70, AtRAD51 and AtRad1, which keeps genome stability in cells of model plant Arabidopsis thaliana, changes differently depending on dose and mode of ionizing radiation exposure had been tested. Gel electrophoresis-based reverse transcription polymerase chain reaction (RT-PCR) method was used for quantifying mRNA transcription levels. The data demonstrated that mode and dose of irradiation affect transcription rate of the genes AtKu70, AtRAD51 and AtRad1. The fractionated and acute X-ray irradiation may result in adaptive response through the induction of key DNA double-strand break (DSB) repair genes AtKu70 and AtRAD51, as well as in genome instability through transcriptional activation of error-prone AtRad1-mediated DNA DSB repair combined with decreased expression of AtRAD51. In plants at doses within the range of 3-9 Gy, an adaptive influence is prevailed, but at doses of 12-21 Gy an error-prone repair of double-strand DNA damage is activated. Fractionation of dose has a significant effect on the transcription of the genes AtKu70, AtRAD51 and AtRad1 only at doses of 15 Gy and 21 Gy. Acute dose of 15 Gy activates error-prone AtRad1-mediated DSB repair and repressed both AtRAD51-dependent and AtKu70-dependent repair pathways, while fractionated irradiation at the same total dose induces more accurate homologous recombination and canonical non-homologous end joining of the DNA strands. In case of A. thaliana exposed to X-rays at dose 21 Gy, the situation is going reversed because of strong induction of the all three genome caretaker genes in leaves of acutely irradiated plants in contrast to the plants under fractionated exposure.

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Comparative Radiation Tolerance Based on the Induction of DNA Double-Strand Breaks in Tobacco BY-2 Cells and CHO-K1 Cells Irradiated with Gamma Rays

Cited by 24 publications

References 30 publications

Ionizing Radiation–dependent γ-H2AX Focus Formation Requires Ataxia Telangiectasia Mutated and Ataxia Telangiectasia Mutated and Rad3-related

Ionizing Radiation–dependent γ-H2AX Focus Formation Requires Ataxia Telangiectasia Mutated and Ataxia Telangiectasia Mutated and Rad3-related

The plant‐specific CDKB 1‐ CYCB 1 complex mediates homologous recombination repair in Arabidopsis

The Transcriptional Response of Arabidopsis thaliana L. Genes AtKu70, AtRAD51 and AtRad1 to X-Ray Radiation

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