scholarly journals Recombinase and translesion DNA polymerase decrease the speed of replication fork progression during the DNA damage response in Escherichia coli cells

2015 ◽  
Vol 43 (3) ◽  
pp. 1714-1725 ◽  
Author(s):  
Kang Wei Tan ◽  
Tuan Minh Pham ◽  
Asako Furukohri ◽  
Hisaji Maki ◽  
Masahiro Tatsumi Akiyama
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Dna Polymerase ◽  
Dna Damage Response ◽  
Replication Fork ◽  
Replication Fork Progression ◽  
Escherichia Coli Cells ◽  
Damage Response ◽  
Translesion Dna

scholarly journals Replication fork dynamics and the DNA damage response

2012 ◽  
Vol 443 (1) ◽  
pp. 13-26 ◽  
Author(s):  
Rebecca M. Jones ◽  
Eva Petermann
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Dna Damage Response ◽  
Replication Fork ◽  
Molecular Mechanisms ◽  
S Phase ◽  
Replication Initiation ◽  
Developmental Defects ◽  
Replication Fork Progression ◽  
Damage Response

Prevention and repair of DNA damage is essential for maintenance of genomic stability and cell survival. DNA replication during S-phase can be a source of DNA damage if endogenous or exogenous stresses impair the progression of replication forks. It has become increasingly clear that DNA-damage-response pathways do not only respond to the presence of damaged DNA, but also modulate DNA replication dynamics to prevent DNA damage formation during S-phase. Such observations may help explain the developmental defects or cancer predisposition caused by mutations in DNA-damage-response genes. The present review focuses on molecular mechanisms by which DNA-damage-response pathways control and promote replication dynamics in vertebrate cells. In particular, DNA damage pathways contribute to proper replication by regulating replication initiation, stabilizing transiently stalled forks, promoting replication restart and facilitating fork movement on difficult-to-replicate templates. If replication fork progression fails to be rescued, this may lead to DNA damage and genomic instability via nuclease processing of aberrant fork structures or incomplete sister chromatid separation during mitosis.

scholarly journals DNA Damage Response Pathway and Replication Fork Stress During Oligonucleotide Directed Gene Editing

2012 ◽  
Vol 1 ◽  
pp. e18 ◽  
Author(s):  
Melissa Bonner ◽  
Bryan Strouse ◽  
Mindy Applegate ◽  
Paula Livingston ◽  
Eric B Kmiec
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Replication Fork ◽  
Gene Editing ◽  
Damage Response ◽  
Dna Damage Response Pathway

scholarly journals Escherichia coli Cells with Increased Levels of DnaA and Deficient in Recombinational Repair Have Decreased Viability

2003 ◽  
Vol 185 (2) ◽  
pp. 630-644 ◽  
Author(s):  
Aline V. Grigorian ◽  
Rachel B. Lustig ◽  
Elena C. Guzmán ◽  
Joseph M. Mahaffy ◽  
Judith W. Zyskind
Keyword(s):  
Escherichia Coli ◽  
Dna Polymerase ◽  
Replication Fork ◽  
Replication Initiation ◽  
Recombinational Repair ◽  
Replication Forks ◽  
Dna Replication Initiation ◽  
Escherichia Coli Cells ◽  
Repair Pathways ◽  
Stalled Replication Forks

ABSTRACT The dnaA operon of Escherichia coli contains the genes dnaA, dnaN, and recF encoding DnaA, β clamp of DNA polymerase III holoenzyme, and RecF. When the DnaA concentration is raised, an increase in the number of DNA replication initiation events but a reduction in replication fork velocity occurs. Because DnaA is autoregulated, these results might be due to the inhibition of dnaN and recF expression. To test this, we examined the effects of increasing the intracellular concentrations of DnaA, β clamp, and RecF, together and separately, on initiation, the rate of fork movement, and cell viability. The increased expression of one or more of the dnaA operon proteins had detrimental effects on the cell, except in the case of RecF expression. A shorter C period was not observed with increased expression of the β clamp; in fact, many chromosomes did not complete replication in runout experiments. Increased expression of DnaA alone resulted in stalled replication forks, filamentation, and a decrease in viability. When the three proteins of the dnaA operon were simultaneously overexpressed, highly filamentous cells were observed (>50 μm) with extremely low viability and, in runout experiments, most chromosomes had not completed replication. The possibility that recombinational repair was responsible for the survival of cells overexpressing DnaA was tested by using mutants in different recombinational repair pathways. The absence of RecA, RecB, RecC, or the proteins in the RuvABC complex caused an additional ∼100-fold drop in viability in cells with increased levels of DnaA, indicating a requirement for recombinational repair in these cells.

scholarly journals Acute MUS81 depletion leads to replication fork slowing and a constitutive DNA damage response

Oncotarget ◽  
2015 ◽  
Vol 6 (35) ◽  
pp. 37638-37646 ◽  
Author(s):  
Meichun Xing ◽  
Xiaohui Wang ◽  
Timea Palmai-Pallag ◽  
Huahao Shen ◽  
Thomas Helleday ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Replication Fork ◽  
Damage Response

scholarly journals p53 suppression overwhelms DNA polymerase η deficiency in determining the cellular UV DNA damage response

DNA Repair ◽  
2007 ◽  
Vol 6 (12) ◽  
pp. 1794-1804 ◽  
Author(s):  
Rebecca R. Laposa ◽  
Luzviminda Feeney ◽  
Eileen Crowley ◽  
Sebastien de Feraudy ◽  
James E. Cleaver
Keyword(s):  
Dna Damage ◽  
Dna Polymerase ◽  
Dna Damage Response ◽  
Damage Response
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