scholarly journals Base excision repair causes age-dependent accumulation of single-stranded DNA breaks that contribute to Parkinson disease pathology

Cell Reports ◽  
2021 ◽  
Vol 36 (10) ◽  
pp. 109668
Author(s):  
Tanima SenGupta ◽  
Konstantinos Palikaras ◽  
Ying Q. Esbensen ◽  
Georgios Konstantinidis ◽  
Francisco Jose Naranjo Galindo ◽  
...  
Keyword(s):  
Parkinson Disease ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Dna Breaks ◽  
Single Stranded Dna ◽  
Age Dependent ◽  
Base Excision

A new DNA breaks repair pathway involving PARP3 and base excision repair proteins

2018 ◽  
Vol 482 (1) ◽  
pp. 96-100
Author(s):  
E. Belousova ◽  
◽  
M. Kutuzov ◽  
P. Ivankina ◽  
A. Ishchenko ◽  
...  
Keyword(s):  
Base Excision Repair ◽  
Excision Repair ◽  
Repair Pathway ◽  
Dna Breaks ◽  
Base Excision

scholarly journals Poly(ADP-ribose) polymerase in base excision repair: always engaged, but not essential for DNA damage processing.

2003 ◽  
Vol 50 (1) ◽  
pp. 169-179 ◽  
Author(s):  
Sarah L Allinson ◽  
Irina I Dianova ◽  
Grigory L Dianov
Keyword(s):  
Dna Damage ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Deficient Mouse ◽  
Dna Breaks ◽  
Abasic Sites ◽  
Cell Extracts ◽  
Mouse Cells ◽  
Base Excision ◽  
Parp 1

Poly(ADP-ribose) polymerase (PARP-1) is an abundant nuclear protein with a high affinity for single- and double-strand DNA breaks. Its binding to strand breaks promotes catalysis of the covalent modification of nuclear proteins with poly(ADP-ribose) synthesised from NAD(+). PARP-1-knockout cells are extremely sensitive to alkylating agents, suggesting the involvement of PARP-1 in base excision repair; however, its role remains unclear. We investigated the dependence of base excision repair pathways on PARP-1 and NAD(+) using whole cell extracts derived from normal and PARP-1 deficient mouse cells and DNA substrates containing abasic sites. In normal extracts the rate of repair was highly dependent on NAD(+). We found that in the absence of NAD(+) repair was slowed down 4-6-fold after incision of the abasic site. We also established that in extracts from PARP-1 deficient mouse cells, repair of both regular and reduced abasic sites was increased with respect to normal extracts and was NAD(+)-independent, suggesting that in both short- and long-patch BER PARP-1 slows down, rather than stimulates, the repair reaction. Our data support the proposal that PARP-1 does not play a major role in catalysis of DNA damage processing via either base excision repair pathway.

scholarly journals DNA breaks and chromosomal aberrations arise when replication meets base excision repair

2014 ◽  
Vol 206 (1) ◽  
pp. 29-43 ◽  
Author(s):  
Michael Ensminger ◽  
Lucie Iloff ◽  
Christian Ebel ◽  
Teodora Nikolova ◽  
Bernd Kaina ◽  
...  
Keyword(s):  
Base Excision Repair ◽  
Chromosomal Aberrations ◽  
Excision Repair ◽  
Double Strand Breaks ◽  
Replication Forks ◽  
Dna Double Strand Breaks ◽  
Dna Breaks ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Base Excision

Exposures that methylate DNA potently induce DNA double-strand breaks (DSBs) and chromosomal aberrations, which are thought to arise when damaged bases block DNA replication. Here, we demonstrate that DNA methylation damage causes DSB formation when replication interferes with base excision repair (BER), the predominant pathway for repairing methylated bases. We show that cells defective in the N-methylpurine DNA glycosylase, which fail to remove N-methylpurines from DNA and do not initiate BER, display strongly reduced levels of methylation-induced DSBs and chromosomal aberrations compared with wild-type cells. Also, cells unable to generate single-strand breaks (SSBs) at apurinic/apyrimidinic sites do not form DSBs immediately after methylation damage. In contrast, cells deficient in x-ray cross-complementing protein 1, DNA polymerase β, or poly (ADP-ribose) polymerase 1 activity, all of which fail to seal SSBs induced at apurinic/apyrimidinic sites, exhibit strongly elevated levels of methylation-induced DSBs and chromosomal aberrations. We propose that DSBs and chromosomal aberrations after treatment with N-alkylators arise when replication forks collide with SSBs generated during BER.

Modulation of Base Excision Repair Alters Cellular Sensitivity to UVA1 but not to UVB¶

2002 ◽  
Vol 75 (5) ◽  
pp. 507 ◽  
Author(s):  
Katherine J. Kim ◽  
Indraneel Chakrabarty ◽  
Guang-Zhi Li ◽  
Sabine Grösch ◽  
Bernd Kaina ◽  
...  
Keyword(s):  
Base Excision Repair ◽  
Excision Repair ◽  
Cellular Sensitivity ◽  
Base Excision

Defective Base Excision Repair Associated with NTHL1

2019 ◽  
Vol 68 ◽  
Author(s):  
Richarda de Voer ◽  
Paul W Doetsch ◽  
Roland Kuiper ◽  
Barbara Rivera
Keyword(s):  
Base Excision Repair ◽  
Excision Repair ◽  
Base Excision
Sign in / Sign up

Export Citation Format

Share Document