scholarly journals Live imaging of induced and controlled DNA double-strand break formation reveals extremely low repair by homologous recombination in human cells

Oncogene ◽  
2011 ◽  
Vol 31 (30) ◽  
pp. 3495-3504 ◽  
Author(s):  
O D Shahar ◽  
E V S Raghu Ram ◽  
E Shimshoni ◽  
S Hareli ◽  
E Meshorer ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Strand Break ◽  
Live Imaging ◽  
Double Strand Break ◽  
Human Cells ◽  
Dna Double Strand Break ◽  
Break Formation

scholarly journals The Over-expression of the β2 Catalytic Subunit of the Proteasome Decreases Homologous Recombination and Impairs DNA Double-Strand Break Repair in Human Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Anita Collavoli ◽  
Laura Comelli ◽  
Tiziana Cervelli ◽  
Alvaro Galli
Keyword(s):  
Homologous Recombination ◽  
Active Role ◽  
Strand Break ◽  
Double Strand Break ◽  
Human Cells ◽  
Proteasome Activity ◽  
Dsb Repair ◽  
Catalytic Subunits ◽  
Over Expression ◽  
Dna Double Strand Break

By a human cDNA library screening, we have previously identified two sequences coding two different catalytic subunits of the proteasome which increase homologous recombination (HR) when overexpressed in the yeastSaccharomyces cerevisiae. Here, we investigated the effect of proteasome on spontaneous HR and DNA repair in human cells. To determine if the proteasome has a role in the occurrence of spontaneous HR in human cells, we overexpressed the β2 subunit of the proteasome in HeLa cells and determined the effect on intrachromosomal HR. Results showed that the overexpression of β2 subunit decreased HR in human cells without altering the cell proteasome activity and the Rad51p level. Moreover, exposure to MG132 that inhibits the proteasome activity reduced HR in human cells. We also found that the expression of the β2 subunit increases the sensitivity to the camptothecin that induces DNA double-strand break (DSB). This suggests that the β2 subunit has an active role in HR and DSB repair but does not alter the intracellular level of the Rad51p.

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 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 Clustered DNA double-strand break formation and the repair pathway following heavy-ion irradiation

2018 ◽  
Vol 60 (1) ◽  
pp. 69-79 ◽  
Author(s):  
Yoshihiko Hagiwara ◽  
Takahiro Oike ◽  
Atsuko Niimi ◽  
Motohiro Yamauchi ◽  
Hiro Sato ◽  
...  
Keyword(s):  
Ion Irradiation ◽  
Heavy Ion ◽  
Strand Break ◽  
Double Strand Break ◽  
Repair Pathway ◽  
Heavy Ion Irradiation ◽  
Dna Double Strand Break ◽  
Break Formation
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