Modulating and Targeting Meiotic Double-Strand Breaks in Saccharomyces cerevisiae

2009 ◽  
pp. 27-33 ◽  
Author(s):  
Alain Nicolas
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
Strand Breaks

scholarly journals Mapping Meiotic Single-Strand DNA Reveals a New Landscape of DNA Double-Strand Breaks in Saccharomyces cerevisiae

PLoS Biology ◽  
2007 ◽  
Vol 5 (12) ◽  
pp. e324 ◽  
Author(s):  
Cyril Buhler ◽  
Valérie Borde ◽  
Michael Lichten
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Dna Double Strand Breaks ◽  
Strand Breaks

scholarly journals Numerical and Spatial Patterning of Yeast Meiotic DNA Breaks by Tel1

2016 ◽  
Author(s):  
Neeman Mohibullah ◽  
Scott Keeney
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Deep Sequencing ◽  
Meiotic Recombination ◽  
Double Strand Breaks ◽  
Genome Integrity ◽  
Spatial Patterning ◽  
Dna Breaks ◽  
Strand Breaks ◽  
Context Dependent

AbstractThe Spo11-generated double-strand breaks (DSBs) that initiate meiotic recombination are dangerous lesions that can disrupt genome integrity, so meiotic cells regulate their number, timing, and distribution. Here, we use Spo11-oligonucleotide complexes, a byproduct of DSB formation, to examine the contribution of the DNA damage-responsive kinase Tel1 (ortholog of mammalian ATM) to this regulation in Saccharomyces cerevisiae. A tel1Δ mutant had globally increased amounts of Spo11-oligonucleotide complexes and altered Spo11-oligonucleotide lengths, consistent with conserved roles for Tel1 in control of DSB number and processing. A kinase-dead tell mutation also increased Spo11-oligonucleotide levels, but mutating known Tel1 phosphotargets on Hop1 and Rec114 did not. Deep sequencing of Spo11 oligonucleotides from tel1Δ mutants demonstrated that Tel1 shapes the nonrandom DSB distribution in ways that are distinct but partially overlapping with previously described contributions of the recombination regulator Zip3. Finally, we uncover a context-dependent role for Tel1 in hotspot competition, in which an artificial DSB hotspot inhibits nearby hotspots. Evidence for Tel1-dependent competition involving strong natural hotspots is also provided.

Roles of Saccharomyces cerevisiae RAD17 and CHK1 checkpoint genes in the repair of double-strand breaks in cycling cells

2007 ◽  
Vol 46 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Nelson Bracesco ◽  
Ema C. Candreva ◽  
Deborah Keszenman ◽  
Ana G. Sánchez ◽  
Sandra Soria ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
Strand Breaks ◽  
Checkpoint Genes

scholarly journals Multiple sites for double-strand breaks in whole meiotic chromosomes of Saccharomyces cerevisiae.

1992 ◽  
Vol 11 (9) ◽  
pp. 3441-3447 ◽  
Author(s):  
D. Zenvirth ◽  
T. Arbel ◽  
A. Sherman ◽  
M. Goldway ◽  
S. Klein ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
Strand Breaks ◽  
Meiotic Chromosomes

scholarly journals Correction: Mapping Meiotic Single-Strand DNA Reveals a New Landscape of DNA Double-Strand Breaks in Saccharomyces cerevisiae

PLoS Biology ◽  
2008 ◽  
Vol 6 (4) ◽  
pp. e104
Author(s):  
Cyril Buhler ◽  
Valérie Borde ◽  
Michael Lichten
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Dna Double Strand Breaks ◽  
Strand Breaks

scholarly journals DNA polymerases δ and λ cooperate in repairing double-strand breaks by microhomology-mediated end-joining in Saccharomyces cerevisiae

2015 ◽  
Vol 112 (50) ◽  
pp. E6907-E6916 ◽  
Author(s):  
Damon Meyer ◽  
Becky Xu Hua Fu ◽  
Wolf-Dietrich Heyer
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Polymerase ◽  
Genome Stability ◽  
Double Strand Breaks ◽  
Dna Polymerase Delta ◽  
Dna Double Strand Breaks ◽  
End Joining ◽  
Strand Breaks ◽  
Repair Efficiency ◽  
Repair Pathways

Maintenance of genome stability is carried out by a suite of DNA repair pathways that ensure the repair of damaged DNA and faithful replication of the genome. Of particular importance are the repair pathways, which respond to DNA double-strand breaks (DSBs), and how the efficiency of repair is influenced by sequence homology. In this study, we developed a genetic assay in diploid Saccharomyces cerevisiae cells to analyze DSBs requiring microhomologies for repair, known as microhomology-mediated end-joining (MMEJ). MMEJ repair efficiency increased concomitant with microhomology length and decreased upon introduction of mismatches. The central proteins in homologous recombination (HR), Rad52 and Rad51, suppressed MMEJ in this system, suggesting a competition between HR and MMEJ for the repair of a DSB. Importantly, we found that DNA polymerase delta (Pol δ) is critical for MMEJ, independent of microhomology length and base-pairing continuity. MMEJ recombinants showed evidence that Pol δ proofreading function is active during MMEJ-mediated DSB repair. Furthermore, mutations in Pol δ and DNA polymerase 4 (Pol λ), the DNA polymerase previously implicated in MMEJ, cause a synergistic decrease in MMEJ repair. Pol λ showed faster kinetics associating with MMEJ substrates following DSB induction than Pol δ. The association of Pol δ depended on RAD1, which encodes the flap endonuclease needed to cleave MMEJ intermediates before DNA synthesis. Moreover, Pol δ recruitment was diminished in cells lacking Pol λ. These data suggest cooperative involvement of both polymerases in MMEJ.

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