scholarly journals Artemis-dependent DNA double-strand break formation at stalled replication forks

2013 ◽  
Vol 104 (6) ◽  
pp. 703-710 ◽  
Author(s):  
Junya Unno ◽  
Masatoshi Takagi ◽  
Jinhua Piao ◽  
Masataka Sugimoto ◽  
Fumiko Honda ◽  
...  
Keyword(s):  
Strand Break ◽  
Double Strand Break ◽  
Replication Forks ◽  
Dna Double Strand Break ◽  
Stalled Replication Forks ◽  
Break Formation

scholarly journals MCL-1 Depletion Impairs DNA Double-Strand Break Repair and Reinitiation of Stalled DNA Replication Forks

2016 ◽  
Vol 37 (3) ◽  
Author(s):  
Abid R. Mattoo ◽  
Raj K. Pandita ◽  
Sharmistha Chakraborty ◽  
Vijaya Charaka ◽  
Kalpana Mujoo ◽  
...  
Keyword(s):  
Myeloid Cell ◽  
Strand Break ◽  
Double Strand Break ◽  
Replication Forks ◽  
Dsb Repair ◽  
Focus Formation ◽  
Hematopoietic Stem ◽  
Dna Double Strand Break ◽  
Dna End Resection ◽  
Stalled Replication Forks

ABSTRACT Myeloid cell leukemia 1 (MCL-1) is a prosurvival BCL-2 protein family member highly expressed in hematopoietic stem cells (HSCs) and regulated by growth factor signals that manifest antiapoptotic activity. Here we report that depletion of MCL-1 but not its isoform MCL-1S increases genomic instability and cell sensitivity to ionizing radiation (IR)-induced death. MCL-1 association with genomic DNA increased postirradiation, and the protein colocalized with 53BP1 foci. Postirradiation, MCL-1-depleted cells exhibited decreased γ-H2AX foci, decreased phosphorylation of ATR, and higher levels of residual 53BP1 and RIF1 foci, suggesting that DNA double-strand break (DSB) repair by homologous recombination (HR) was compromised. Consistent with this model, MCL-1-depleted cells had a reduced frequency of IR-induced BRCA1, RPA, and Rad51 focus formation, decreased DNA end resection, and decreased HR repair in the DR-GFP DSB repair model. Similarly, after HU induction of stalled replication forks in MCL-1-depleted cells, there was a decreased ability to subsequently restart DNA synthesis, which is normally dependent upon HR-mediated resolution of collapsed forks. Therefore, the present data support a model whereby MCL-1 depletion increases 53BP1 and RIF1 colocalization at DSBs, which inhibits BRCA1 recruitment, and sensitizes cells to DSBs from IR or stalled replication forks that require HR for repair.

scholarly journals Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination

2021 ◽  
Author(s):  
Kyosuke Nakamura ◽  
Georg Kustatscher ◽  
Constance Alabert ◽  
Martina Hödl ◽  
Ignasi Forne ◽  
...  
Keyword(s):  
Strand Break ◽  
Double Strand Break ◽  
Replication Forks ◽  
Dna 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

Release of paused RNA polymerase II at specific loci favors DNA double-strand-break formation and promotes cancer translocations

2019 ◽  
Vol 51 (6) ◽  
pp. 1011-1023 ◽  
Author(s):  
Gaetano Ivan Dellino ◽  
Fernando Palluzzi ◽  
Andrea Maria Chiariello ◽  
Rossana Piccioni ◽  
Simona Bianco ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Strand Break ◽  
Double Strand Break ◽  
Dna Double Strand Break ◽  
Break Formation
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