Bacterial Proliferation: Keep Dividing and Don't Mind the Gap

Bacterial Proliferation: Keep Dividing and Don't Mind the Gap

DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies showed that the bacterial replicase is able to re-prime downstream of a DNA lesion, leaving behind a single-stranded DNA gap. The question r...

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Published in:PLoS genetics Vol. 11; no. 12; p. e1005757
Main Authors: Laureti, Luisa, Demol, Julien, Fuchs, Robert P, Pagès, Vincent
Format: Journal Article
Language:English
Published: United States Public Library of Science 01-12-2015
Public Library of Science (PLoS)
Subjects:
Biochemistry, Molecular Biology
Cell Division
Cell proliferation
Chromosomes
DNA Breaks, Single-Stranded
DNA Damage
DNA repair
DNA sequencing
Escherichia coli - genetics
Escherichia coli - physiology
Escherichia coli Proteins - genetics
Escherichia coli Proteins - metabolism
Life Sciences
Methods
Molecular biology
Nucleotide sequencing
Observations
Plasmids
Rec A Recombinases - genetics
Rec A Recombinases - metabolism
Recombinational DNA Repair
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Abstract DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies showed that the bacterial replicase is able to re-prime downstream of a DNA lesion, leaving behind a single-stranded DNA gap. The question remains of what happens to this gap in vivo. Following the insertion of a single lesion in the chromosome of a living cell, we showed that this gap is mostly filled in by Homology Directed Gap Repair in a RecA dependent manner. When cells fail to repair this gap, or when homologous recombination is impaired, cells are still able to divide, leading to the loss of the damaged chromatid, suggesting that bacteria lack a stringent cell division checkpoint mechanism. Hence, at the expense of losing one chromatid, cell survival and proliferation are ensured.
AbstractList DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies showed that the bacterial replicase is able to re-prime downstream of a DNA lesion, leaving behind a single-stranded DNA gap. The question remains of what happens to this gap in vivo. Following the insertion of a single lesion in the chromosome of a living cell, we showed that this gap is mostly filled in by Homology Directed Gap Repair in a RecA dependent manner. When cells fail to repair this gap, or when homologous recombination is impaired, cells are still able to divide, leading to the loss of the damaged chromatid, suggesting that bacteria lack a stringent cell division checkpoint mechanism. Hence, at the expense of losing one chromatid, cell survival and proliferation are ensured. Author Summary DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication, thus challenging genome integrity. Two DDT mechanisms have previously been described: error prone Translesion Synthesis operated by specialized DNA polymerases and error free bypass that uses the information of the sister chromatid to bypass the lesion. In this work, we set up a novel genetic system that allows to insert a single DNA blocking lesion in the chromosome of a living cell and to visualize the exchange of genetic information between the undamaged and the damaged strand. Using this system, we showed in vivo that the replication fork is able to re-prime downstream of the lesion, leaving a gap. This gap is mostly filled in by the error free pathway through the RecA homologous recombination mechanism. We show that when the gap is left unre-paired, cells are still able to divide by losing the damaged chromatid, which evidences the lack of a stringent cell division checkpoint system.
DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies showed that the bacterial replicase is able to re-prime downstream of a DNA lesion, leaving behind a single-stranded DNA gap. The question remains of what happens to this gap in vivo . Following the insertion of a single lesion in the chromosome of a living cell, we showed that this gap is mostly filled in by Homology Directed Gap Repair in a RecA dependent manner. When cells fail to repair this gap, or when homologous recombination is impaired, cells are still able to divide, leading to the loss of the damaged chromatid, suggesting that bacteria lack a stringent cell division checkpoint mechanism. Hence, at the expense of losing one chromatid, cell survival and proliferation are ensured. DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication, thus challenging genome integrity. Two DDT mechanisms have previously been described: error prone Translesion Synthesis operated by specialized DNA polymerases and error free bypass that uses the information of the sister chromatid to bypass the lesion. In this work, we set up a novel genetic system that allows to insert a single DNA blocking lesion in the chromosome of a living cell and to visualize the exchange of genetic information between the undamaged and the damaged strand. Using this system, we showed in vivo that the replication fork is able to re-prime downstream of the lesion, leaving a gap. This gap is mostly filled in by the error free pathway through the RecA homologous recombination mechanism. We show that when the gap is left unrepaired, cells are still able to divide by losing the damaged chromatid, which evidences the lack of a stringent cell division checkpoint system.
DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies showed that the bacterial replicase is able to re-prime downstream of a DNA lesion, leaving behind a singlestranded DNA gap. The question remains of what happens to this gap in vivo. Following the insertion of a single lesion in the chromosome of a living cell, we showed that this gap is mostly filled in by Homology Directed Gap Repair in a RecA dependent manner. When cells fail to repair this gap, or when homologous recombination is impaired, cells are still able to divide, leading to the loss of the damaged chromatid, suggesting that bacteria lack a stringent cell division checkpoint mechanism. Hence, at the expense of losing one chromatid, cell survival and proliferation are ensured.
DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies showed that the bacterial replicase is able to re-prime downstream of a DNA lesion, leaving behind a single-stranded DNA gap. The question remains of what happens to this gap in vivo. Following the insertion of a single lesion in the chromosome of a living cell, we showed that this gap is mostly filled in by Homology Directed Gap Repair in a RecA dependent manner. When cells fail to repair this gap, or when homologous recombination is impaired, cells are still able to divide, leading to the loss of the damaged chromatid, suggesting that bacteria lack a stringent cell division checkpoint mechanism. Hence, at the expense of losing one chromatid, cell survival and proliferation are ensured.
  DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies showed that the bacterial replicase is able to re-prime downstream of a DNA lesion, leaving behind a single-stranded DNA gap. The question remains of what happens to this gap in vivo. Following the insertion of a single lesion in the chromosome of a living cell, we showed that this gap is mostly filled in by Homology Directed Gap Repair in a RecA dependent manner. When cells fail to repair this gap, or when homologous recombination is impaired, cells are still able to divide, leading to the loss of the damaged chromatid, suggesting that bacteria lack a stringent cell division checkpoint mechanism. Hence, at the expense of losing one chromatid, cell survival and proliferation are ensured.
Audience Academic
Author Pagès, Vincent
Fuchs, Robert P
Laureti, Luisa
Demol, Julien
AuthorAffiliation University of Michigan, UNITED STATES
Cancer Research Center of Marseille, Team DNA Damage Tolerance, CNRS, UMR7258; Inserm, U1068; Institut Paoli-Calmettes; Aix-Marseille University, Marseille, France
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Cites_doi 10.1016/0022-2836(86)90273-1
10.1073/pnas.0608293104
10.1101/gad.417607
10.4161/23723548.2014.957039
10.1016/0014-5793(85)80266-0
10.1101/gad.1780709
10.1128/MMBR.63.4.751-813.1999
10.1093/emboj/19.22.6259
10.1038/sj.emboj.7601474
10.1038/35044005
10.1128/9781555817640.ch21
10.1016/0022-2836(89)90259-3
10.1128/JB.97.3.1134-1141.1969
10.1016/j.jmb.2008.06.031
10.1038/sj.onc.1206006
10.1093/genetics/160.3.851
10.1016/0022-2836(68)90445-2
10.1128/JB.182.23.6598-6604.2000
10.1016/0092-8674(93)90493-A
10.1016/0005-2787(71)90551-X
10.1016/j.molcel.2005.11.015
10.1093/nar/gks675
10.1038/nature04329
10.1016/S0300-9084(97)82002-0
10.1038/emboj.2013.211
10.1371/journal.pgen.0030226
10.1128/JB.181.2.508-520.1999
10.1128/JB.156.3.1093-1098.1983
10.3389/fgene.2013.00026
10.1073/pnas.120163297
10.1046/j.1365-2443.2003.00646.x
10.1128/JB.187.6.1974-1984.2005
10.1016/0022-2836(76)90156-X
10.1016/j.dnarep.2009.04.014
10.1126/science.1081328
10.1128/MMBR.00020-08
10.1016/j.molcel.2013.10.020
10.1038/ncomms7357
10.1016/S0092-8674(00)80621-2
10.1073/pnas.1321008111
10.1073/pnas.59.2.598
10.1016/j.jmb.2013.07.021
10.1016/j.mrrev.2015.02.001
10.1126/science.1083964
10.1002/bies.20233
10.1016/j.dnarep.2006.07.002
10.1074/jbc.M112.397034
10.1038/nrm3935
10.1126/science.1209111
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Conceived and designed the experiments: LL VP. Performed the experiments: LL JD. Analyzed the data: LL VP. Wrote the paper: LL VP RPF.
The authors have declared that no competing interests exist.
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References NP Higgins (ref5) 1976; 101
N Handa (ref22) 2009; 23
BE Dutra (ref27) 2007; 104
K Morimatsu (ref35) 2012; 287
L Sandell (ref41) 1993; 75
V Pagès (ref1) 2002; 21
GA Pandya (ref12) 2000; 182
M Inuzuka (ref47) 1985; 181
S Mohebi (ref42) 2015; 6
VN Iyer (ref28) 1971; 228
TC Wang (ref36) 1983; 156
V Pagès (ref15) 2003; 300
R Napolitano (ref23) 2000; 19
L Amado (ref30) 2013; 425
RC Heller (ref32) 2006; 439
BB Zhou (ref38) 2000; 408
M Spies (ref21) 2005
T-CV Wang (ref10) 2005; 27
F Prado (ref2) 2014; 1
X Xu (ref3) 2015; 764
R Okazaki (ref29) 1968; 59
KA Datsenko (ref45) 2000; 97
K Naiman (ref18) 2014; 111
D Branzei (ref39) 2009; 8
AI Ozgenc (ref13) 2005; 187
M Lopes (ref31) 2006; 21
P Koehl (ref49) 1989; 207
CE Bauer (ref48) 1986; 192
WD Rupp (ref4) 1968; 31
J Courcelle (ref7) 2003; 299
MS Dillingham (ref20) 2008; 72
P McGlynn (ref6) 2000; 101
K Higuchi (ref16) 2003; 8
S Autret (ref37) 1997; 79
V Pagès (ref17) 2012; 40
ST Lovett (ref26) 2002; 160
CJ Rudolph (ref8) 2007; 21
KJ Neelsen (ref9) 2015; 16
HW Mankouri (ref43) 2013; 32
JTP Yeeles (ref33) 2011; 334
DS Weiss (ref46) 1999; 181
A Kuzminov (ref19) 1999; 63
L Izhar (ref14) 2008; 381
S Fujii (ref24) 2006; 25
AR Lehmann (ref11) 2006; 5
P Howard-Flanders (ref25) 1969; 97
E Esnault (ref44) 2007; 3
JTP Yeeles (ref34) 2013; 52
R Jossen (ref40) 2013; 4
References_xml – volume: 192
  start-page: 513
  year: 1986
  ident: ref48
  article-title: Mutational analysis of integrase arm-type binding sites of bacteriophage lambda. Integration and excision involve distinct interactions of integrase with arm-type sites
  publication-title: Journal of Molecular Biology
  doi: 10.1016/0022-2836(86)90273-1
  contributor:
    fullname: CE Bauer
– volume: 104
  start-page: 216
  year: 2007
  ident: ref27
  article-title: RecA-independent recombination is efficient but limited by exonucleases
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.0608293104
  contributor:
    fullname: BE Dutra
– volume: 21
  start-page: 668
  year: 2007
  ident: ref8
  article-title: Replication fork stalling and cell cycle arrest in UV-irradiated Escherichia coli
  publication-title: Genes Dev
  doi: 10.1101/gad.417607
  contributor:
    fullname: CJ Rudolph
– volume: 1
  start-page: e957039
  year: 2014
  ident: ref2
  article-title: Homologous recombination maintenance of genome integrity during DNA damage tolerance
  publication-title: Molecular & Cellular Oncology
  doi: 10.4161/23723548.2014.957039
  contributor:
    fullname: F Prado
– volume: 181
  start-page: 236
  year: 1985
  ident: ref47
  article-title: Plasmid-encoded initiation protein is required for activity at all three origins of plasmid R6K DNA replication in vitro
  publication-title: FEBS Lett
  doi: 10.1016/0014-5793(85)80266-0
  contributor:
    fullname: M Inuzuka
– volume: 23
  start-page: 1234
  year: 2009
  ident: ref22
  article-title: Reconstitution of initial steps of dsDNA break repair by the RecF pathway of E. coli
  publication-title: Genes Dev
  doi: 10.1101/gad.1780709
  contributor:
    fullname: N Handa
– volume: 63
  start-page: 751
  year: 1999
  ident: ref19
  article-title: Recombinational repair of DNA damage in Escherichia coli and bacteriophage lambda
  publication-title: Microbiol Mol Biol Rev
  doi: 10.1128/MMBR.63.4.751-813.1999
  contributor:
    fullname: A Kuzminov
– volume: 19
  start-page: 6259
  year: 2000
  ident: ref23
  article-title: All three SOS-inducible DNA polymerases (Pol II, Pol IV and Pol V) are involved in induced mutagenesis
  publication-title: EMBO J
  doi: 10.1093/emboj/19.22.6259
  contributor:
    fullname: R Napolitano
– volume: 25
  start-page: 5754
  year: 2006
  ident: ref24
  article-title: RecFOR proteins are essential for Pol V-mediated translesion synthesis and mutagenesis
  publication-title: EMBO J
  doi: 10.1038/sj.emboj.7601474
  contributor:
    fullname: S Fujii
– volume: 408
  start-page: 433
  year: 2000
  ident: ref38
  article-title: The DNA damage response: putting checkpoints in perspective
  publication-title: Nature
  doi: 10.1038/35044005
  contributor:
    fullname: BB Zhou
– start-page: 389
  year: 2005
  ident: ref21
  article-title: Homologous recombination by RecBCD and RecF pathways
  publication-title: The bacterial chromosome
  doi: 10.1128/9781555817640.ch21
  contributor:
    fullname: M Spies
– volume: 207
  start-page: 355
  year: 1989
  ident: ref49
  article-title: Construction of plasmids containing a unique acetylaminofluorene adduct located within a mutation hot spot. A new probe for frameshift mutagenesis
  publication-title: Journal of Molecular Biology
  doi: 10.1016/0022-2836(89)90259-3
  contributor:
    fullname: P Koehl
– volume: 97
  start-page: 1134
  year: 1969
  ident: ref25
  article-title: Some properties of excision-defective recombination-deficient mutants of Escherichia coli K-12
  publication-title: J Bacteriol
  doi: 10.1128/JB.97.3.1134-1141.1969
  contributor:
    fullname: P Howard-Flanders
– volume: 381
  start-page: 803
  year: 2008
  ident: ref14
  article-title: Analysis of strand transfer and template switching mechanisms of DNA gap repair by homologous recombination in Escherichia coli: predominance of strand transfer
  publication-title: Journal of Molecular Biology
  doi: 10.1016/j.jmb.2008.06.031
  contributor:
    fullname: L Izhar
– volume: 21
  start-page: 8957
  year: 2002
  ident: ref1
  article-title: How DNA lesions are turned into mutations within cells?
  publication-title: Oncogene
  doi: 10.1038/sj.onc.1206006
  contributor:
    fullname: V Pagès
– volume: 160
  start-page: 851
  year: 2002
  ident: ref26
  article-title: Crossing over between regions of limited homology in Escherichia coli. RecA-dependent and RecA-independent pathways
  publication-title: Genetics
  doi: 10.1093/genetics/160.3.851
  contributor:
    fullname: ST Lovett
– volume: 31
  start-page: 291
  year: 1968
  ident: ref4
  article-title: Discontinuities in the DNA synthesized in an excision-defective strain of Escherichia coli following ultraviolet irradiation
  publication-title: Journal of Molecular Biology
  doi: 10.1016/0022-2836(68)90445-2
  contributor:
    fullname: WD Rupp
– volume: 182
  start-page: 6598
  year: 2000
  ident: ref12
  article-title: Escherichia coli responses to a single DNA adduct
  publication-title: J Bacteriol
  doi: 10.1128/JB.182.23.6598-6604.2000
  contributor:
    fullname: GA Pandya
– volume: 75
  start-page: 729
  year: 1993
  ident: ref41
  article-title: Loss of a yeast telomere: Arrest, recovery, and chromosome loss
  publication-title: Cell
  doi: 10.1016/0092-8674(93)90493-A
  contributor:
    fullname: L Sandell
– volume: 228
  start-page: 117
  year: 1971
  ident: ref28
  article-title: Usefulness of benzoylated naphthoylated DEAE-cellulose to distinguish and fractionate double-stranded DNA bearing different extents of single-stranded regions
  publication-title: Biochim Biophys Acta
  doi: 10.1016/0005-2787(71)90551-X
  contributor:
    fullname: VN Iyer
– volume: 21
  start-page: 15
  year: 2006
  ident: ref31
  article-title: Multiple mechanisms control chromosome integrity after replication fork uncoupling and restart at irreparable UV lesions
  publication-title: Molecular Cell
  doi: 10.1016/j.molcel.2005.11.015
  contributor:
    fullname: M Lopes
– volume: 40
  start-page: 9036
  year: 2012
  ident: ref17
  article-title: Monitoring bypass of single replication-blocking lesions by damage avoidance in the Escherichia coli chromosome
  publication-title: Nucleic Acids Research
  doi: 10.1093/nar/gks675
  contributor:
    fullname: V Pagès
– volume: 439
  start-page: 557
  year: 2006
  ident: ref32
  article-title: Replication fork reactivation downstream of a blocked nascent leading strand
  publication-title: Nature
  doi: 10.1038/nature04329
  contributor:
    fullname: RC Heller
– volume: 79
  start-page: 549
  year: 1997
  ident: ref37
  article-title: Cell cycle checkpoints in bacteria
  publication-title: Biochimie
  doi: 10.1016/S0300-9084(97)82002-0
  contributor:
    fullname: S Autret
– volume: 32
  start-page: 2661
  year: 2013
  ident: ref43
  article-title: How unfinished business from S-phase affects mitosis and beyond
  publication-title: EMBO J
  doi: 10.1038/emboj.2013.211
  contributor:
    fullname: HW Mankouri
– volume: 3
  start-page: e226
  year: 2007
  ident: ref44
  article-title: Chromosome structuring limits genome plasticity in Escherichia coli
  publication-title: PLoS Genet
  doi: 10.1371/journal.pgen.0030226
  contributor:
    fullname: E Esnault
– volume: 181
  start-page: 508
  year: 1999
  ident: ref46
  article-title: Localization of FtsI (PBP3) to the septal ring requires its membrane anchor, the Z ring, FtsA, FtsQ, and FtsL
  publication-title: J Bacteriol
  doi: 10.1128/JB.181.2.508-520.1999
  contributor:
    fullname: DS Weiss
– volume: 156
  start-page: 1093
  year: 1983
  ident: ref36
  article-title: Mechanisms for recF-dependent and recB-dependent pathways of postreplication repair in UV-irradiated Escherichia coli uvrB
  publication-title: J Bacteriol
  doi: 10.1128/JB.156.3.1093-1098.1983
  contributor:
    fullname: TC Wang
– volume: 4
  start-page: 26
  year: 2013
  ident: ref40
  article-title: . The DNA damage checkpoint response to replication stress: A Game of Forks
  publication-title: Front Genet
  doi: 10.3389/fgene.2013.00026
  contributor:
    fullname: R Jossen
– volume: 97
  start-page: 6640
  year: 2000
  ident: ref45
  article-title: One-step inactivation of chromosomal genes in Escherichia coli K-12 using PCR products
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.120163297
  contributor:
    fullname: KA Datsenko
– volume: 8
  start-page: 437
  year: 2003
  ident: ref16
  article-title: Fate of DNA replication fork encountering a single DNA lesion during oriC plasmid DNA replication in vitro
  publication-title: Genes Cells
  doi: 10.1046/j.1365-2443.2003.00646.x
  contributor:
    fullname: K Higuchi
– volume: 187
  start-page: 1974
  year: 2005
  ident: ref13
  article-title: In vivo evidence for a recA-independent recombination process in Escherichia coli that permits completion of replication of DNA containing UV damage in both strands
  publication-title: J Bacteriol
  doi: 10.1128/JB.187.6.1974-1984.2005
  contributor:
    fullname: AI Ozgenc
– volume: 101
  start-page: 417
  year: 1976
  ident: ref5
  article-title: A model for replication repair in mammalian cells
  publication-title: Journal of Molecular Biology
  doi: 10.1016/0022-2836(76)90156-X
  contributor:
    fullname: NP Higgins
– volume: 8
  start-page: 1038
  year: 2009
  ident: ref39
  article-title: The checkpoint response to replication stress
  publication-title: DNA Repair
  doi: 10.1016/j.dnarep.2009.04.014
  contributor:
    fullname: D Branzei
– volume: 299
  start-page: 1064
  year: 2003
  ident: ref7
  article-title: DNA damage-induced replication fork regression and processing in Escherichia coli
  publication-title: Science
  doi: 10.1126/science.1081328
  contributor:
    fullname: J Courcelle
– volume: 72
  start-page: 642
  year: 2008
  ident: ref20
  article-title: RecBCD enzyme and the repair of double-stranded DNA breaks
  publication-title: Microbiol Mol Biol Rev
  doi: 10.1128/MMBR.00020-08
  contributor:
    fullname: MS Dillingham
– volume: 52
  start-page: 855
  year: 2013
  ident: ref34
  article-title: Dynamics of leading-strand lesion skipping by the replisome
  publication-title: Molecular Cell
  doi: 10.1016/j.molcel.2013.10.020
  contributor:
    fullname: JTP Yeeles
– volume: 6
  start-page: 6357
  year: 2015
  ident: ref42
  article-title: Checkpoints are blind to replication restart and recombination intermediates that result in gross chromosomal rearrangements
  publication-title: Nat Commun
  doi: 10.1038/ncomms7357
  contributor:
    fullname: S Mohebi
– volume: 101
  start-page: 35
  year: 2000
  ident: ref6
  article-title: Modulation of RNA polymerase by (p)ppGpp reveals a RecG-dependent mechanism for replication fork progression
  publication-title: Cell
  doi: 10.1016/S0092-8674(00)80621-2
  contributor:
    fullname: P McGlynn
– volume: 111
  start-page: 5526
  year: 2014
  ident: ref18
  article-title: Chronology in lesion tolerance gives priority to genetic variability
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.1321008111
  contributor:
    fullname: K Naiman
– volume: 59
  start-page: 598
  year: 1968
  ident: ref29
  article-title: Mechanism of DNA chain growth. I. Possible discontinuity and unusual secondary structure of newly synthesized chains
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.59.2.598
  contributor:
    fullname: R Okazaki
– volume: 425
  start-page: 4177
  year: 2013
  ident: ref30
  article-title: Low-molecular-weight DNA replication intermediates in Escherichia coli: mechanism of formation and strand specificity
  publication-title: Journal of Molecular Biology
  doi: 10.1016/j.jmb.2013.07.021
  contributor:
    fullname: L Amado
– volume: 764
  start-page: 43
  year: 2015
  ident: ref3
  article-title: Error-free DNA-damage tolerance in Saccharomyces cerevisiae
  publication-title: Mutat Res Rev Mutat Res
  doi: 10.1016/j.mrrev.2015.02.001
  contributor:
    fullname: X Xu
– volume: 300
  start-page: 1300
  year: 2003
  ident: ref15
  article-title: Uncoupling of leading- and lagging-strand DNA replication during lesion bypass in vivo
  publication-title: Science
  doi: 10.1126/science.1083964
  contributor:
    fullname: V Pagès
– volume: 27
  start-page: 633
  year: 2005
  ident: ref10
  article-title: Discontinuous or semi-discontinuous DNA replication in Escherichia coli?
  publication-title: Bioessays
  doi: 10.1002/bies.20233
  contributor:
    fullname: T-CV Wang
– volume: 5
  start-page: 1495
  year: 2006
  ident: ref11
  article-title: Gaps and forks in DNA replication: Rediscovering old models
  publication-title: DNA Repair
  doi: 10.1016/j.dnarep.2006.07.002
  contributor:
    fullname: AR Lehmann
– volume: 287
  start-page: 35621
  year: 2012
  ident: ref35
  article-title: RecFOR proteins target RecA protein to a DNA gap with either DNA or RNA at the 5' terminus: implication for repair of stalled replication forks
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M112.397034
  contributor:
    fullname: K Morimatsu
– volume: 16
  start-page: 207
  year: 2015
  ident: ref9
  article-title: Replication fork reversal in eukaryotes: from dead end to dynamic response
  publication-title: Nat Rev Mol Cell Biol
  doi: 10.1038/nrm3935
  contributor:
    fullname: KJ Neelsen
– volume: 334
  start-page: 235
  year: 2011
  ident: ref33
  article-title: The Escherichia coli replisome is inherently DNA damage tolerant
  publication-title: Science
  doi: 10.1126/science.1209111
  contributor:
    fullname: JTP Yeeles
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Snippet DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies...
DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies...
  DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro...
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StartPage e1005757
SubjectTerms Biochemistry, Molecular Biology
Cell Division
Cell proliferation
Chromosomes
DNA Breaks, Single-Stranded
DNA Damage
DNA repair
DNA sequencing
Escherichia coli - genetics
Escherichia coli - physiology
Escherichia coli Proteins - genetics
Escherichia coli Proteins - metabolism
Life Sciences
Methods
Molecular biology
Nucleotide sequencing
Observations
Plasmids
Rec A Recombinases - genetics
Rec A Recombinases - metabolism
Recombinational DNA Repair
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Title Bacterial Proliferation: Keep Dividing and Don't Mind the Gap
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