A Comparative Study of Rejoining of DNA Double-strand Breaks in Yeast Irradiated with 3·5 MeV α-particles or with 30 MeV Electrons

Frankenberg-Schwager, M.; Frankenberg, D.; Harbich, R.; Adamczyk, C.

doi:10.1080/09553009014551261

Cited by 47 publications

(5 citation statements)

References 19 publications

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“…These considerations further indicate that the radicals leading to DSB should derive from one single and not from two or more independent ionisation events occurring directly adjacent to the DNA backbone. Consequently, DSB induction should be a linear function of dose as shown in many irradiation experiments performed in vivo or in solution [1,32,33] and in the present communication (Fig. 2).…”

Section: Discussionsupporting

confidence: 66%

Pulsed-field gel electrophoresis of chromosomal DNA of Saccharomyces pastorianus after exposure to x-rays (30-50 keV) and neutrons (14 MeV)

Potter¹,

Köhnlein²

2001

Radiation and Environmental Biophysics

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Chromosomes of budding yeast Saccharomyces pastorianus were used to determine the extent of DNA double-strand breaks (DSBs) induced by x-rays (30-50 keV) and 14 MeV neutrons. The yeast chromosomes were separated by pulsed-field gel electrophoresis (PFGE) and the proportion of unbroken molecules corresponding to the largest chromosome no. IV (1500 kbp) was used to calculate the DSB frequency assuming a random distribution of hits. To determine the protective contribution of the cell environment, chromosomes embedded in agarose plugs as well as intact yeast cells, were irradiated under conditions completely inhibiting DNA repair. Following irradiation, the intact cells were also embedded in agarose plugs and the chromosomes isolated to perform PFGE. All radiation experiments resulted in a linear dose-effect curve for DSBs. For both radiation qualities, the yield of DSBs for exposed isolated chromosomes exceeded that for intact yeast cells by a factor of 13. The relative biological effectiveness (RBE) of 14 MeV neutrons in the induction of DNA DSBs was about 2.5. This figure was found to be identical for the in vivo and in vitro exposure of yeast chromosomes (neutrons 36.7 and 2.8, x-rays 14.5 and 1.1 x 10(-8) DSB x Bp-1 Gy-1 for isolated DNA and intact cells, respectively).

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Section: Discussionsupporting

confidence: 66%

Pulsed-field gel electrophoresis of chromosomal DNA of Saccharomyces pastorianus after exposure to x-rays (30-50 keV) and neutrons (14 MeV)

Potter¹,

Köhnlein²

2001

Radiation and Environmental Biophysics

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“…The CFGE and PFGE experiments illustrate the kinetics of DSB repair for cells irradiated with photons and ions [135,157,169,174,. PFGE assays have been used to study the effect of repair protein mutation [146,147] or radiation quality [179,187,199] on repair kinetics.…”

Section: Gel Electrophoresismentioning

confidence: 99%

A kinetic model of single-strand annealing for the repair of DNA double-strand breaks

Taleei

Weinfeld

Nikjoo

2010

Radiation Protection Dosimetry

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Ionising radiation induces different types of DNA damage, including single-strand breaks, double-strand breaks (DSB) and base damages. DSB are considered to be the most critical lesion to be repaired. The three main competitive pathways in the repair of DSB are non-homologous end joining (NHEJ), homologous recombination (HR) and single-strand annealing (SSA). SSA is a non-conservative repair pathway requiring direct repeat sequences for the repair process. In this work, a biochemical kinetic model is presented to describe the SSA repair pathway. The model consists of a system of non-linear ordinary differential equations describing the steps in the repair pathway. The reaction rates were estimated by comparing the model results with the experimental data for chicken DT40 cells exposed to 20 Gy of X-rays. The model successfully predicts the repair of the DT40 cells with the reaction rates derived from the 20-Gy X-ray experiment. The experimental data and the kinetic model show fast and slow DSB repair components. The half time and fractions of the slow and the fast components of the repair were compared for the model and the experiments. Mathematical and computational modelling in biology has played an important role in predicting biological mechanisms and stimulating future experimentation. The present model of SSA adds to the modelling of NHEJ and HR to provide a more complete description of DSB repair pathways.

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“…Studies of the kinetics of double-strand break repair show a rapid initial reduction with a tail at longer times which invariably reveals a proportion of breaks which are unrepaired. This repair has been analysed in terms of exponential functions representing fast and slow repair processes (Frankenberg-Schwager 1990, Frankenberg-Schwager et al 1990, Jenner et al 1993, Kysela et al 1993, Sternlow et al 1994, 2000, Dahm-Daphi and Dikomey 1996, Greinert et al 1996, Belli et al 2000, Ahnstrom et al 2000 but has also been analysed in terms of a spectrum of repair probabilities (Foray et al 1998) as well as a bimolecular reaction rate, which is probably closer to the actual repair processes going on in the cell (Fowler 1999, Cucinotta et al 2000. It must be noted that the measurements of repair of DNA double-strand breaks are made of necessity at high radiation doses as the measurement techniques are not sensitive enough to measure the few remaining unrepaired breaks if experiments are done at doses of direct significance for radiological protection.…”

Section: Repair Of Dna Double-strand Breaksmentioning

confidence: 99%

A contribution to the linear no-threshold discussion

2003

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The paper approaches the linear no-threshold (LNT) hypothesis, currently used as the basis for recommendations in radiological protection, from the point of view of the radiation mechanism. All considerations of the validity of the LNT hypothesis based on experiment or epidemiology are dismissed because of the impossibility of deriving statistically significant data at very low doses. Instead, the LNT hypothesis is assessed from a consideration of the mechanism of radiation action. The DNA double-strand break is proposed to be the crucial radiation-induced molecular lesion. A trace is made using a series of correlations that link the DNA double-strand break to effects at the cellular level and these cellular effects are linked to the induction of cancer. Multistep modelling of carcinogenesis is used to take the link through to a consideration of radiation risk. It is concluded that, from the point of view of radiation mechanism, at very low doses the LNT hypothesis of radiation action is valid, that is, the risk function has a positive slope from zero dose.

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A Comparative Study of Rejoining of DNA Double-strand Breaks in Yeast Irradiated with 3·5 MeV α-particles or with 30 MeV Electrons

Cited by 47 publications

References 19 publications

Pulsed-field gel electrophoresis of chromosomal DNA of Saccharomyces pastorianus after exposure to x-rays (30-50 keV) and neutrons (14 MeV)

Pulsed-field gel electrophoresis of chromosomal DNA of Saccharomyces pastorianus after exposure to x-rays (30-50 keV) and neutrons (14 MeV)

A kinetic model of single-strand annealing for the repair of DNA double-strand breaks

A contribution to the linear no-threshold discussion

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