ArticleGenetics1998
Radiation-induced chromosome aberrations in Saccharomyces cerevisiae: influence of DNA repair pathways.
Article in Genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Article
- Biochemical and biomolecular effects induced by a static magnetic field in Saccharomyces cerevisiae: Evidence for oxidative stress.PloS one · 2019Article
- Inactivation of RAD52 and HDF1 DNA repair genes leads to premature chronological aging and cellular instability.Journal of biosciences · 2017Article
- Ionizing irradiation-induced radical stress stalls live meiotic chromosome movements by altering the actin cytoskeleton.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The proteasome factor Bag101 binds to Rad22 and suppresses homologous recombination.Scientific reports · 2013Article
- Double-strand breaks associated with repetitive DNA can reshape the genome.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- HDF1 and RAD17 genes are involved in DNA double-strand break repair in stationary phase Saccharomyces cerevisiae.Journal of biological physics · 2008Article
- Roles of Saccharomyces cerevisiae RAD17 and CHK1 checkpoint genes in the repair of double-strand breaks in cycling cells.Radiation and environmental biophysics · 2007Article
- Fission yeast Rhp51 is required for the maintenance of telomere structure in the absence of the Ku heterodimer.Nucleic acids research · 2003Article
- Homologous recombination is essential for RAD51 up-regulation in Saccharomyces cerevisiae following DNA crosslinking damage.Nucleic acids research · 2002Article
- Ku and the Stability of the Genome.Journal of biomedicine & biotechnology · 2002Article
- DNA integration by Ty integrase in yku70 mutant Saccharomyces cerevisiae cells.Molecular and cellular biology · 2000Article
- Subtelomeric repeat amplification is associated with growth at elevated temperature in yku70 mutants of Saccharomyces cerevisiae.Genetics · 2000Article
- DNA damage-inducible and RAD52-independent repair of DNA double-strand breaks in Saccharomyces cerevisiae.Genetics · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiation-induced chromosome aberrations, particularly exchange-type aberrations, are thought to result from misrepair of DNA double-strand breaks. The relationship between individual pathways of break repair and aberration formation is not clear. By electrophoretic karyotyping of single-cell clones derived from irradiated cells, we have analyzed the induction of stable aberrations in haploid yeast cells mutated for the RAD52 gene, the RAD54 gene, the HDF1(= YKU70) gene, or combinations thereof. We found low and comparable frequencies of aberrational events in wildtype and hdf1 mutants, and assume that in these strains most of the survivors descended from cells that were in G2 phase during irradiation and therefore able to repair breaks by homologous recombination between sister chromatids. In the rad52 and the rad54 strains, enhanced formation of aberrations, mostly exchange-type aberrations, was detected, demonstrating the misrepair activity of a rejoining mechanism other than homologous recombination. No aberration was found in the rad52 hdf1 double mutant, and the frequency in the rad54 hdf1 mutant was very low. Hence, misrepair resulting in exchange-type aberrations depends largely on the presence of Hdf1, a component of the nonhomologous end-joining pathway in yeast.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.