Repair of double-strand breaks in plasmid DNA in the yeast Saccharomyces cerevisiae

1988 ◽  
Vol 213 (2-3) ◽  
pp. 421-424 ◽  
Author(s):  
Joseph R. Perera ◽  
Alexander V. Glasunov ◽  
Vadim M. Glaser ◽  
Alla V. Boreiko
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Plasmid Dna ◽  
Double Strand Breaks ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks

scholarly journals Repair of Endonuclease-Induced Double-Strand Breaks in Saccharomyces cerevisiae: Essential Role for Genes Associated with Nonhomologous End-Joining

Genetics ◽  
1999 ◽  
Vol 152 (4) ◽  
pp. 1513-1529 ◽  
Author(s):  
L Kevin Lewis ◽  
James W Westmoreland ◽  
Michael A Resnick
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Excision Repair ◽  
Cell Killing ◽  
Double Strand Breaks ◽  
Nonhomologous End Joining ◽  
Chromosomal Dna ◽  
End Joining ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks

Abstract Repair of double-strand breaks (DSBs) in chromosomal DNA by nonhomologous end-joining (NHEJ) is not well characterized in the yeast Saccharomyces cerevisiae. Here we demonstrate that several genes associated with NHEJ perform essential functions in the repair of endonuclease-induced DSBs in vivo. Galactose-induced expression of EcoRI endonuclease in rad50, mre11, or xrs2 mutants, which are deficient in plasmid DSB end-joining and some forms of recombination, resulted in G2 arrest and rapid cell killing. Endonuclease synthesis also produced moderate cell killing in sir4 strains. In contrast, EcoRI caused prolonged cell-cycle arrest of recombination-defective rad51, rad52, rad54, rad55, and rad57 mutants, but cells remained viable. Cell-cycle progression was inhibited in excision repair-defective rad1 mutants, but not in rad2 cells, indicating a role for Rad1 processing of the DSB ends. Phenotypic responses of additional mutants, including exo1, srs2, rad5, and rdh54 strains, suggest roles in recombinational repair, but not in NHEJ. Interestingly, the rapid cell killing in haploid rad50 and mre11 strains was largely eliminated in diploids, suggesting that the cohesive-ended DSBs could be efficiently repaired by homologous recombination throughout the cell cycle in the diploid mutants. These results demonstrate essential but separable roles for NHEJ pathway genes in the repair of chromosomal DSBs that are structurally similar to those occurring during cellular development.

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 Hypermutability of Damaged Single-Strand DNA Formed at Double-Strand Breaks and Uncapped Telomeres in Yeast Saccharomyces cerevisiae

PLoS Genetics ◽  
2008 ◽  
Vol 4 (11) ◽  
pp. e1000264 ◽  
Author(s):  
Yong Yang ◽  
Joan Sterling ◽  
Francesca Storici ◽  
Michael A. Resnick ◽  
Dmitry A. Gordenin
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks

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 Multiple Pathways of Recombination Induced by Double-Strand Breaks in Saccharomyces cerevisiae

1999 ◽  
Vol 63 (2) ◽  
pp. 349-404 ◽  
Author(s):  
Frédéric Pâques ◽  
James E. Haber
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Genetic Recombination ◽  
Double Strand Breaks ◽  
Molecular Models ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks ◽  
The Past ◽  
Biochemical Studies

SUMMARY The budding yeast Saccharomyces cerevisiae has been the principal organism used in experiments to examine genetic recombination in eukaryotes. Studies over the past decade have shown that meiotic recombination and probably most mitotic recombination arise from the repair of double-strand breaks (DSBs). There are multiple pathways by which such DSBs can be repaired, including several homologous recombination pathways and still other nonhomologous mechanisms. Our understanding has also been greatly enriched by the characterization of many proteins involved in recombination and by insights that link aspects of DNA repair to chromosome replication. New molecular models of DSB-induced gene conversion are presented. This review encompasses these different aspects of DSB-induced recombination in Saccharomyces and attempts to relate genetic, molecular biological, and biochemical studies of the processes of DNA repair and recombination.

scholarly journals Isolation of COM1, a New Gene Required to Complete Meiotic Double-Strand Break-Induced Recombination in Saccharomyces cerevisiae

Genetics ◽  
1997 ◽  
Vol 146 (3) ◽  
pp. 781-795 ◽  
Author(s):  
Susanne Prinz ◽  
Angelika Amon ◽  
Franz Klein
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Strand Break ◽  
Double Strand Breaks ◽  
Homologous Pairing ◽  
Yeast Saccharomyces Cerevisiae ◽  
Spore Viability ◽  
Strand Breaks ◽  
New Gene ◽  
Synaptonemal Complex Formation

We have designed a screen to isolate mutants defective during a specific part of meiotic prophase I of the yeast Saccharomyces cerevisiae. Genes required for the repair of meiotic double-strand breaks or for the separation of recombined chromosomes are targets of this mutant hunt. The specificity is achieved by selecting for mutants that produce viable spores when recombination and reductional segregation are prevented by mutations in SPO11 and SP013 genes, but fail to yield viable spores during a normal Rec+ meiosis. We have identified and characterized a mutation com1-1, which blocks processing of meiotic double-strand breaks and which interferes with synaptonemal complex formation, homologous pairing and, as a consequence, spore viability after induction of meiotic recombination. The COM1/SAE2 gene was cloned by complementation, and the deletion mutant has a phenotype similar to com1-1. com1/sae2 mutants closely resemble the phenotype of rad50S, as assayed by phase-contrast microscopy for spore formation, physical and genetic analysis of recombination, fluorescence in situ hybridization to quantify homologous pairing and immunofluorescence and electron microscopy to determine the capability to synapse axial elements.

Genetic control of plasmid DNA double-strand gap repair in yeast, Saccharomyces cerevisiae

1990 ◽  
Vol 18 (1) ◽  
pp. 1-5 ◽  
Author(s):  
V. M. Glaser ◽  
A. V. Glasunov ◽  
G. G. Tevzadze ◽  
J. R. Perera ◽  
S. V. Shestakov
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Genetic Control ◽  
Plasmid Dna ◽  
Yeast Saccharomyces Cerevisiae
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