Faculty Opinions recommendation of The processivity factor beta controls DNA polymerase IV traffic during spontaneous mutagenesis and translesion synthesis in vivo.

2002 ◽  
Author(s):  
Errol C Friedberg
Keyword(s):  
Dna Polymerase ◽  
Translesion Synthesis ◽  
Spontaneous Mutagenesis ◽  
Processivity Factor ◽  
Dna Polymerase Iv

scholarly journals The processivity factor β controls DNA polymerase IV traffic during spontaneous mutagenesis and translesion synthesis in vivo

EMBO Reports ◽  
2002 ◽  
Vol 3 (1) ◽  
pp. 45-49 ◽  
Author(s):  
Nathalie Lenne‐Samuel ◽  
Jérôme Wagner ◽  
Hélène Etienne ◽  
Robert P P Fuchs
Keyword(s):  
Dna Polymerase ◽  
Translesion Synthesis ◽  
Spontaneous Mutagenesis ◽  
Processivity Factor ◽  
Dna Polymerase Iv

scholarly journals Interactions and Localization of Escherichia coli Error-Prone DNA Polymerase IV after DNA Damage

2015 ◽  
Vol 197 (17) ◽  
pp. 2792-2809 ◽  
Author(s):  
Sarita Mallik ◽  
Ellen M. Popodi ◽  
Andrew J. Hanson ◽  
Patricia L. Foster
Keyword(s):  
Dna Damage ◽  
Dna Polymerase ◽  
Dna Helicase ◽  
Dna Lesions ◽  
Replication Forks ◽  
Content Type ◽  
Pol Iv ◽  
Dna Polymerase Iv ◽  
Stalled Replication Forks

ABSTRACTEscherichia coli's DNA polymerase IV (Pol IV/DinB), a member of the Y family of error-prone polymerases, is induced during the SOS response to DNA damage and is responsible for translesion bypass and adaptive (stress-induced) mutation. In this study, the localization of Pol IV after DNA damage was followed using fluorescent fusions. After exposure ofE. colito DNA-damaging agents, fluorescently tagged Pol IV localized to the nucleoid as foci. Stepwise photobleaching indicated ∼60% of the foci consisted of three Pol IV molecules, while ∼40% consisted of six Pol IV molecules. Fluorescently tagged Rep, a replication accessory DNA helicase, was recruited to the Pol IV foci after DNA damage, suggesting that thein vitrointeraction between Rep and Pol IV reported previously also occursin vivo. Fluorescently tagged RecA also formed foci after DNA damage, and Pol IV localized to them. To investigate if Pol IV localizes to double-strand breaks (DSBs), an I-SceI endonuclease-mediated DSB was introduced close to a fluorescently labeled LacO array on the chromosome. After DSB induction, Pol IV localized to the DSB site in ∼70% of SOS-induced cells. RecA also formed foci at the DSB sites, and Pol IV localized to the RecA foci. These results suggest that Pol IV interacts with RecAin vivoand is recruited to sites of DSBs to aid in the restoration of DNA replication.IMPORTANCEDNA polymerase IV (Pol IV/DinB) is an error-prone DNA polymerase capable of bypassing DNA lesions and aiding in the restart of stalled replication forks. In this work, we demonstratein vivolocalization of fluorescently tagged Pol IV to the nucleoid after DNA damage and to DNA double-strand breaks. We show colocalization of Pol IV with two proteins: Rep DNA helicase, which participates in replication, and RecA, which catalyzes recombinational repair of stalled replication forks. Time course experiments suggest that Pol IV recruits Rep and that RecA recruits Pol IV. These findings providein vivoevidence that Pol IV aids in maintaining genomic stability not only by bypassing DNA lesions but also by participating in the restoration of stalled replication forks.

Synthesis of N2-Deoxyguanosine Modified DNAs and the Studies on Their Translesion Synthesis by the E. coli DNA Polymerase IV

2019 ◽  
Vol 84 (4) ◽  
pp. 1734-1747 ◽  
Author(s):  
Pratibha P. Ghodke ◽  
Praneeth Bommisetti ◽  
Deepak T. Nair ◽  
P. I. Pradeepkumar
Keyword(s):  
Dna Polymerase ◽  
Translesion Synthesis ◽  
E Coli ◽  
Dna Polymerase Iv

scholarly journals Single-molecule live-cell imaging reveals RecB-dependent function of DNA polymerase IV in double strand break repair

2020 ◽  
Vol 48 (15) ◽  
pp. 8490-8508 ◽  
Author(s):  
Sarah S Henrikus ◽  
Camille Henry ◽  
Amy E McGrath ◽  
Slobodan Jergic ◽  
John P McDonald ◽  
...  
Keyword(s):  
Dna Polymerase ◽  
Single Molecule ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Breaks ◽  
Strand Breaks ◽  
E Coli ◽  
Pol Iv ◽  
Dna Polymerase Iv

Abstract Several functions have been proposed for the Escherichia coli DNA polymerase IV (pol IV). Although much research has focused on a potential role for pol IV in assisting pol III replisomes in the bypass of lesions, pol IV is rarely found at the replication fork in vivo. Pol IV is expressed at increased levels in E. coli cells exposed to exogenous DNA damaging agents, including many commonly used antibiotics. Here we present live-cell single-molecule microscopy measurements indicating that double-strand breaks induced by antibiotics strongly stimulate pol IV activity. Exposure to the antibiotics ciprofloxacin and trimethoprim leads to the formation of double strand breaks in E. coli cells. RecA and pol IV foci increase after treatment and exhibit strong colocalization. The induction of the SOS response, the appearance of RecA foci, the appearance of pol IV foci and RecA-pol IV colocalization are all dependent on RecB function. The positioning of pol IV foci likely reflects a physical interaction with the RecA* nucleoprotein filaments that has been detected previously in vitro. Our observations provide an in vivo substantiation of a direct role for pol IV in double strand break repair in cells treated with double strand break-inducing antibiotics.

scholarly journals Analysis of Damage Tolerance Pathways in Saccharomyces cerevisiae: a Requirement for Rev3 DNA Polymerase in Translesion Synthesis

1998 ◽  
Vol 18 (2) ◽  
pp. 960-966 ◽  
Author(s):  
K. Baynton ◽  
A. Bresson-Roy ◽  
R. P. P. Fuchs
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Polymerase ◽  
Excision Repair ◽  
Translesion Synthesis ◽  
Hybridization Technique ◽  
Nucleotide Excision ◽  
Yeast Transformants ◽  
Plasmid Design ◽  
First Time

ABSTRACT The replication of double-stranded plasmids containing a singleN-2-acetylaminofluorene (AAF) adduct located in a short, heteroduplex sequence was analyzed in Saccharomyces cerevisiae. The strains used were proficient or deficient for the activity of DNA polymerase ζ (REV3 andrev3Δ, respectively) in a mismatch and nucleotide excision repair-defective background (msh2Δ rad10Δ). The plasmid design enabled the determination of the frequency with which translesion synthesis (TLS) and mechanisms avoiding the adduct by using the undamaged, complementary strand (damage avoidance mechanisms) are invoked to complete replication. To this end, a hybridization technique was implemented to probe plasmid DNA isolated from individual yeast transformants by using short, 32P-end-labeled oligonucleotides specific to each strand of the heteroduplex. In both the REV3 and rev3Δ strains, the two strands of an unmodified heteroduplex plasmid were replicated in ∼80% of the transformants, with the remaining 20% having possibly undergone prereplicative MSH2-independent mismatch repair. However, in the presence of the AAF adduct, TLS occurred in only 8% of theREV3 transformants, among which 97% was mostly error free and only 3% resulted in a mutation. All TLS observed in theREV3 strain was abolished in the rev3Δ mutant, providing for the first time in vivo biochemical evidence of a requirement for the Rev3 protein in TLS.

scholarly journals REV1 restrains DNA polymerase ζ to ensure frame fidelity during translesion synthesis of UV photoproducts in vivo

2008 ◽  
Vol 36 (21) ◽  
pp. 6767-6780 ◽  
Author(s):  
Dávid Szüts ◽  
Adam P. Marcus ◽  
Masayuki Himoto ◽  
Shigenori Iwai ◽  
Julian E. Sale
Keyword(s):  
Dna Polymerase ◽  
Translesion Synthesis ◽  
Uv Photoproducts

scholarly journals PrimPol is required for replication reinitiation after mtDNA damage

2017 ◽  
Vol 114 (43) ◽  
pp. 11398-11403 ◽  
Author(s):  
Rubén Torregrosa-Muñumer ◽  
Josefin M. E. Forslund ◽  
Steffi Goffart ◽  
Annika Pfeiffer ◽  
Gorazd Stojkovič ◽  
...  
Keyword(s):  
Dna Polymerase ◽  
Translesion Synthesis ◽  
Replication Forks ◽  
Mtdna Damage ◽  
Replicative Stress ◽  
Mtdna Replication ◽  
Stalled Replication Forks ◽  
Lagging Strand

Eukaryotic PrimPol is a recently discovered DNA-dependent DNA primase and translesion synthesis DNA polymerase found in the nucleus and mitochondria. Although PrimPol has been shown to be required for repriming of stalled replication forks in the nucleus, its role in mitochondria has remained unresolved. Here we demonstrate in vivo and in vitro that PrimPol can reinitiate stalled mtDNA replication and can prime mtDNA replication from nonconventional origins. Our results not only help in the understanding of how mitochondria cope with replicative stress but can also explain some controversial features of the lagging-strand replication.

scholarly journals Role of Escherichia coli DNA Polymerase IV in In Vivo Replication Fidelity

2004 ◽  
Vol 186 (14) ◽  
pp. 4802-4807 ◽  
Author(s):  
Wojciech Kuban ◽  
Piotr Jonczyk ◽  
Damian Gawel ◽  
Karolina Malanowska ◽  
Roel M. Schaaper ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Mismatch Repair ◽  
Dna Polymerase ◽  
Error Rate ◽  
The Other ◽  
Chromosomal Dna ◽  
Pol Iv ◽  
Dna Polymerase Iv

ABSTRACT We have investigated whether DNA polymerase IV (Pol IV; the dinB gene product) contributes to the error rate of chromosomal DNA replication in Escherichia coli. We compared mutation frequencies in mismatch repair-defective strains that were either dinB positive or dinB deficient, using a series of mutational markers, including lac targets in both orientations on the chromosome. Virtually no contribution of Pol IV to the chromosomal mutation rate was observed. On the other hand, a significant effect of dinB was observed for reversion of a lac allele when the lac gene resided on an F′(pro-lac) episome.

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