Repair of MMS-induced DNA double-strand breaks in haploid cells of Saccharomyces cerevisiae, which requires the presence of a duplicate genome

1979 ◽  
Vol 167 (3) ◽  
pp. 279-286 ◽  
Author(s):  
E. Chlebowicz ◽  
W. J. Jachymczyk
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
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.

Cell-Cycle-Specific Repair of DNA Double-Strand Breaks in Saccharomyces cerevisiae

1980 ◽  
Vol 82 (3) ◽  
pp. 547 ◽  
Author(s):  
Gunnar Brunborg ◽  
Michael A. Resnick ◽  
Donald H. Williamson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks

scholarly journals A multistep genomic screen identifies new genes required for repair of DNA double-strand breaks in Saccharomyces cerevisiae

BMC Genomics ◽  
2013 ◽  
Vol 14 (1) ◽  
pp. 251 ◽  
Author(s):  
Jennifer Summers McKinney ◽  
Sunaina Sethi ◽  
Jennifer DeMars Tripp ◽  
Thuy N Nguyen ◽  
Brian A Sanderson ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
New Genes ◽  
Genomic Screen

scholarly journals Blunt-ended DNA double-strand breaks induced by endonucleases PvuII and EcoRV are poor substrates for repair in Saccharomyces cerevisiae

DNA Repair ◽  
2010 ◽  
Vol 9 (6) ◽  
pp. 617-626 ◽  
Author(s):  
James W. Westmoreland ◽  
Jennifer A. Summers ◽  
Cory L. Holland ◽  
Michael A. Resnick ◽  
L. Kevin Lewis
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks

scholarly journals Saccharomyces cerevisiae Mhr1 can bind Xho I-induced mitochondrial DNA double-strand breaks in vivo

Mitochondrion ◽  
2018 ◽  
Vol 42 ◽  
pp. 23-32 ◽  
Author(s):  
Kanchanjunga Prasai ◽  
Lucy C. Robinson ◽  
Kelly Tatchell ◽  
Lynn Harrison
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Dna ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks

scholarly journals A sharp Pif1-dependent threshold separates DNA double-strand breaks from critically short telomeres

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Jonathan Strecker ◽  
Sonia Stinus ◽  
Mariana Pliego Caballero ◽  
Rachel K Szilard ◽  
Michael Chang ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage Response ◽  
Transition Point ◽  
Repeat Sequence ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Telomerase Inhibitor ◽  
Damage Response ◽  
Pif1 Helicase

DNA double-strand breaks (DSBs) and short telomeres are structurally similar, yet they have diametrically opposed fates. Cells must repair DSBs while blocking the action of telomerase on these ends. Short telomeres must avoid recognition by the DNA damage response while promoting telomerase recruitment. In Saccharomyces cerevisiae, the Pif1 helicase, a telomerase inhibitor, lies at the interface of these end-fate decisions. Using Pif1 as a sensor, we uncover a transition point in which 34 bp of telomeric (TG1-3)n repeat sequence renders a DNA end insensitive to Pif1 action, thereby enabling extension by telomerase. A similar transition point exists at natural chromosome ends, where telomeres shorter than ~40 bp are inefficiently extended by telomerase. This phenomenon is not due to known Pif1 modifications and we instead propose that Cdc13 renders TG34+ ends insensitive to Pif1 action. We contend that the observed threshold of Pif1 activity defines a dividing line between DSBs and telomeres.

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