scholarly journals The role of double-strand break-induced allelic homologous recombination in somatic plant cells

2002 ◽  
Vol 32 (3) ◽  
pp. 277-284 ◽  
Author(s):  
Brigitte Gisler ◽  
Siegfried Salomon ◽  
Holger Puchta
Keyword(s):  
Homologous Recombination ◽  
Plant Cells ◽  
Strand Break ◽  
Double Strand Break

The role of homologous recombination in radiation-induced double-strand break repair

2011 ◽  
Vol 101 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Penny A. Jeggo ◽  
Verena Geuting ◽  
Markus Löbrich
Keyword(s):  
Homologous Recombination ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Radiation Induced ◽  
Break Repair

scholarly journals The Mre11-Rad50-Xrs2 Protein Complex Facilitates Homologous Recombination-Based Double-Strand Break Repair inSaccharomyces cerevisiae

1999 ◽  
Vol 19 (11) ◽  
pp. 7681-7687 ◽  
Author(s):  
Debra A. Bressan ◽  
Bonnie K. Baxter ◽  
John H. J. Petrini
Keyword(s):  
Homologous Recombination ◽  
Sister Chromatid ◽  
Protein Complex ◽  
Cellular Response ◽  
Strand Break ◽  
Double Strand Break ◽  
Dsb Repair ◽  
Synchronous Cultures ◽  
Dna Dsbs

ABSTRACT Saccharomyces cerevisiae mre11Δ mutants are profoundly deficient in double-strand break (DSB) repair, indicating that the Mre11-Rad50-Xrs2 protein complex plays a central role in the cellular response to DNA DSBs. In this study, we examined the role of the complex in homologous recombination, the primary mode of DSB repair in yeast. We measured survival in synchronous cultures following irradiation and scored sister chromatid and interhomologue recombination genetically. mre11Δ strains were profoundly sensitive to ionizing radiation (IR) throughout the cell cycle. Mutant strains exhibited decreased frequencies of IR-induced sister chromatid and interhomologue recombination, indicating a general deficiency in homologous recombination-based DSB repair. Since a nuclease-deficientmre11 mutant was not impaired in these assays, it appears that the role of the S. cerevisiae Mre11-Rad50-Xrs2 protein complex in facilitating homologous recombination is independent of its nuclease activities.

scholarly journals Formation of Large Palindromic DNA by Homologous Recombination of Short Inverted Repeat Sequences in Saccharomyces cerevisiae

Genetics ◽  
2002 ◽  
Vol 161 (3) ◽  
pp. 1065-1075
Author(s):  
David K Butler ◽  
David Gillespie ◽  
Brandi Steele
Keyword(s):  
Homologous Recombination ◽  
Inverted Repeat ◽  
Excision Repair ◽  
Strand Break ◽  
Double Strand Break ◽  
Repeat Sequence ◽  
Inverted Repeat Sequence ◽  
Repeat Sequences ◽  
Dna Double Strand Break ◽  
Intermolecular Reaction

Abstract Large DNA palindromes form sporadically in many eukaryotic and prokaryotic genomes and are often associated with amplified genes. The presence of a short inverted repeat sequence near a DNA double-strand break has been implicated in the formation of large palindromes in a variety of organisms. Previously we have established that in Saccharomyces cerevisae a linear DNA palindrome is efficiently formed from a single-copy circular plasmid when a DNA double-strand break is introduced next to a short inverted repeat sequence. In this study we address whether the linear palindromes form by an intermolecular reaction (that is, a reaction between two identical fragments in a head-to-head arrangement) or by an unusual intramolecular reaction, as it apparently does in other examples of palindrome formation. Our evidence supports a model in which palindromes are primarily formed by an intermolecular reaction involving homologous recombination of short inverted repeat sequences. We have also extended our investigation into the requirement for DNA double-strand break repair genes in palindrome formation. We have found that a deletion of the RAD52 gene significantly reduces palindrome formation by intermolecular recombination and that deletions of two other genes in the RAD52-epistasis group (RAD51 and MRE11) have little or no effect on palindrome formation. In addition, palindrome formation is dramatically reduced by a deletion of the nucleotide excision repair gene RAD1.

scholarly journals Double strand break repair by homologous recombination is regulated by cell cycle-independent signaling via ATM in human glioma cells. Vol. 279 (2004) 15402-15410

2004 ◽  
Vol 279 (23) ◽  
pp. 24906
Author(s):  
Sarah E. Golding ◽  
Elizabeth Rosenberg ◽  
Ashraf Khalil ◽  
Alison McEwen ◽  
Matthew Holmes ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Homologous Recombination ◽  
Glioma Cells ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Break Repair

scholarly journals Genetic Analysis of the DNA-dependent Protein Kinase Reveals an Inhibitory Role of Ku in Late S–G2Phase DNA Double-strand Break Repair

2001 ◽  
Vol 276 (48) ◽  
pp. 44413-44418 ◽  
Author(s):  
Toru Fukushima ◽  
Minoru Takata ◽  
Ciaran Morrison ◽  
Ryoko Araki ◽  
Akira Fujimori ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Genetic Analysis ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Dependent Protein Kinase ◽  
Inhibitory Role ◽  
Dna Double Strand Break ◽  
Dependent Protein

Double-strand break repair and homologous recombination inSchizosaccharomyces pombe

Yeast ◽  
2006 ◽  
Vol 23 (13) ◽  
pp. 963-976 ◽  
Author(s):  
Hayatu Raji ◽  
Edgar Hartsuiker
Keyword(s):  
Homologous Recombination ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Break Repair

scholarly journals Schizosaccharomyces pombe KAT5 contributes to resection and repair of a DNA double strand break

Genetics ◽  
2021 ◽  
Author(s):  
Tingting Li ◽  
Ruben C Petreaca ◽  
Susan L Forsburg
Keyword(s):  
Dna Damage ◽  
Homologous Recombination ◽  
Chromatin Remodeling ◽  
Dna Damage Response ◽  
Histone Acetyltransferase ◽  
Strand Break ◽  
Double Strand Break ◽  
Dna Damage Checkpoint ◽  
Dna Double Strand Break ◽  
Damage Response

Abstract Chromatin remodeling is essential for effective repair of a DNA double strand break. KAT5 (S. pombe Mst1, human TIP60) is a MYST family histone acetyltransferase conserved from yeast to humans that coordinates various DNA damage response activities at a DNA double strand break (DSB), including histone remodeling and activation of the DNA damage checkpoint. In S. pombe, mutations in mst1+ causes sensitivity to DNA damaging drugs. Here we show that Mst1 is recruited to DSBs. Mutation of mst1+ disrupts recruitment of repair proteins and delays resection. These defects are partially rescued by deletion of pku70, which has been previously shown to antagonize repair by homologous recombination. These phenotypes of mst1 are similar to pht1-4KR, a non-acetylatable form of histone variant H2A.Z, which has been proposed to affect resection. Our data suggest that Mst1 functions to direct repair of DSBs towards homologous recombination pathways by modulating resection at the double strand break.

scholarly journals The Role of Double-Strand Break Repair Pathways at Functional and Dysfunctional Telomeres

2014 ◽  
Vol 6 (12) ◽  
pp. a016576-a016576 ◽  
Author(s):  
Y. Doksani ◽  
T. de Lange
Keyword(s):  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Repair Pathways ◽  
Break Repair
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