A rapid method to monitor repair and mis-repair of DNA double-strand breaks by using cell extracts of the yeast Saccharomyces cerevisiae

1998 ◽  
Vol 33 (1) ◽  
pp. 1-3 ◽  
Author(s):  
Bhavanath Jha ◽  
F. Ahne ◽  
Manfred Kistler ◽  
Christian Klaus ◽  
Friederike Eckardt-Schupp
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Rapid Method ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks ◽  
Cell Extracts

scholarly journals The Saccharomyces cerevisiae Ku Autoantigen Homologue Affects Radiosensitivity Only in the Absence of Homologous Recombination

Genetics ◽  
1996 ◽  
Vol 142 (1) ◽  
pp. 91-102 ◽  
Author(s):  
Wolfram Siede ◽  
Anna A Friedl ◽  
Irina Dianova ◽  
Friederike Eckardt-Schupp ◽  
Errol C Friedberg
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Homologous Recombination ◽  
Ionizing Radiation ◽  
Mammalian Cells ◽  
Cell Cycle Checkpoint ◽  
Double Strand Breaks ◽  
Minor Importance ◽  
Dna Double Strand Breaks ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks

In mammalian cells, all subunits of the DNA-dependent protein kinase (DNA-PK) have been implicated in the repair of DNA double-strand breaks and in V(D)J recombination. In the yeast Saccharomyces cerevisiae, we have examined the phenotype conferred by a deletion of HDF1, the putative homologue of the 70-kD subunit of the DNA-end binding Ku complex of DNA-PK. The yeast gene does not play a role in radiation-induced cell cycle checkpoint arrest in G1 and G2 or in hydroxyurea-induced checkpoint arrest in S. In cells competent for homologous recombination, we could not detect any sensitivity to ionizing radiation or to methyl methanesulfonate (MMS) conferred by a hdf1 deletion and indeed, the repair of DNA double-strand breaks was not impaired. However, if homologous recombination was disabled (rad52 mutant background), inactivation of HDF1 results in additional sensitization toward ionizing radiation and MMS. These results give further support to the notion that, in contrast to higher eukaryotic cells, homologous recombination is the favored pathway of double-strand break repair in yeast whereas other competing mechanisms such as the suggested pathway of DNA-PK-dependent direct break rejoining are only of minor importance.

Cisplatin-mediated DNA double-strand breaks in replicating but not in quiescent cells of the yeast Saccharomyces cerevisiae

Toxicology ◽  
2005 ◽  
Vol 212 (2-3) ◽  
pp. 175-184 ◽  
Author(s):  
Marlis Frankenberg-Schwager ◽  
Dorothea Kirchermeier ◽  
Goetz Greif ◽  
Karin Baer ◽  
Manuela Becker ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks ◽  
Quiescent Cells

scholarly journals Genetic Interactions of Histone Modification Machinery Set1 and PAF1C with the Recombination Complex Rec114-Mer2-Mei4 in the Formation of Meiotic DNA Double-Strand Breaks

2020 ◽  
Vol 21 (8) ◽  
pp. 2679
Author(s):  
Ying Zhang ◽  
Takuya Suzuki ◽  
Ke Li ◽  
Santosh K. Gothwal ◽  
Miki Shinohara ◽  
...  
Keyword(s):  
Histone Modification ◽  
Genetic Interaction ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
H3k4 Methylation ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks ◽  
Histone H3k4 ◽  
Genomic Locations ◽  
Chromosome Axis

Homologous recombination is essential for chromosome segregation during meiosis I. Meiotic recombination is initiated by the introduction of double-strand breaks (DSBs) at specific genomic locations called hotspots, which are catalyzed by Spo11 and its partners. DSB hotspots during meiosis are marked with Set1-mediated histone H3K4 methylation. The Spo11 partner complex, Rec114-Mer2-Mei4, essential for the DSB formation, localizes to the chromosome axes. For efficient DSB formation, a hotspot with histone H3K4 methylation on the chromatin loops is tethered to the chromosome axis through the H3K4 methylation reader protein, Spp1, on the axes, which interacts with Mer2. In this study, we found genetic interaction of mutants in a histone modification protein complex called PAF1C with the REC114 and MER2 in the DSB formation in budding yeast Saccharomyces cerevisiae. Namely, the paf1c mutations rtf1 and cdc73 showed synthetic defects in meiotic DSB formation only when combined with a wild-type-like tagged allele of either the REC114 or MER2. The synthetic defect of the tagged REC114 allele in the DSB formation was seen also with the set1, but not with spp1 deletion. These results suggest a novel role of histone modification machinery in DSB formation during meiosis, which is independent of Spp1-mediated loop-axis tethering.

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