scholarly journals Role of the Rep Helicase Gene in Homologous Recombination in Neisseria gonorrhoeae

2005 ◽  
Vol 187 (8) ◽  
pp. 2903-2907 ◽  
Author(s):  
Kimberly A. Kline ◽  
H. Steven Seifert
Keyword(s):  
Escherichia Coli ◽  
Dna Repair ◽  
Homologous Recombination ◽  
Neisseria Gonorrhoeae ◽  
Replication Fork ◽  
Dna Transformation ◽  
Replication Fork Progression ◽  
Helicase Gene ◽  
Replication Restart

ABSTRACT In Escherichia coli, the Rep helicase has been implicated in replication fork progression, replication restart, homologous recombination, and DNA repair. We show that a Neisseria gonorrhoeae rep mutant is deficient in the homologous-recombination-mediated processes of DNA transformation and pilus-based colony variation but not in DNA repair.

scholarly journals Roles of the recJ and recN Genes in Homologous Recombination and DNA Repair Pathways of Neisseria gonorrhoeae

2002 ◽  
Vol 184 (4) ◽  
pp. 919-927 ◽  
Author(s):  
Eric P. Skaar ◽  
Matthew P. Lazio ◽  
H. Steven Seifert
Keyword(s):  
Dna Repair ◽  
Homologous Recombination ◽  
Neisseria Gonorrhoeae ◽  
Transformation Efficiency ◽  
Dna Transformation ◽  
Loss Of Function ◽  
Repair Ability ◽  
Dependent Processes ◽  
Strain Fa1090

ABSTRACT The paradigm of homologous recombination comes from Escherichia coli, where the genes involved have been segregated into pathways. In the human pathogen Neisseria gonorrhoeae (the gonococcus), the pathways of homologous recombination are being delineated. To investigate the roles of the gonococcal recN and recJ genes in the recombination-based processes of the gonococcus, these genes were inactivated in the N. gonorrhoeae strain FA1090. We report that both recN and recJ loss-of-function mutants show decreased DNA repair ability. In addition, the recJ mutant was decreased in pilus-dependent colony morphology variation frequency but not DNA transformation efficiency, while the recN mutant was decreased in DNA transformation efficiency but not pilus-dependent variation frequency. We were able to complement all of these deficiencies by supplying an ectopic functional copy of either recJ or recN at an irrelevant locus. These results describe the role of recJ and recN in the recombination-dependent processes of the gonococcus and further define the pathways of homologous recombination in this organism.

scholarly journals Mutation of the priA Gene of Neisseria gonorrhoeae Affects DNA Transformation and DNA Repair

2005 ◽  
Vol 187 (15) ◽  
pp. 5347-5355 ◽  
Author(s):  
Kimberly A. Kline ◽  
H. Steven Seifert
Keyword(s):  
Dna Repair ◽  
Neisseria Gonorrhoeae ◽  
Parental Strain ◽  
Antigenic Variation ◽  
Cumene Hydroperoxide ◽  
Dna Transformation ◽  
Chromosomal Replication ◽  
Replication Fork Progression ◽  
Growth Deficiency

ABSTRACT In Escherichia coli, PriA is central to the restart of chromosomal replication when replication fork progression is disrupted and is also involved in homologous recombination and DNA repair. To investigate the role of PriA in recombination and repair in Neisseria gonorrhoeae, we identified, cloned, and insertionally inactivated the gonococcal priA homologue. The priA mutant showed a growth deficiency and decreased DNA repair capability and was completely for deficient in DNA transformation compared to the isogenic parental strain. The priA mutant was also more sensitive to the oxidative damaging agents H2O2 and cumene hydroperoxide compared to the parental strain. These phenotypes were complemented by supplying a functional copy of priA elsewhere in the chromosome. The N. gonorrhoeae priA mutant showed no alteration in the frequency of pilin antigenic variation. We conclude that PriA participates in DNA repair and DNA transformation processes but not in pilin antigenic variation.

scholarly journals The structure-specific endonuclease complex SLX4/XPF regulates Tus/Ter-induced homologous recombination

2021 ◽  
Author(s):  
Ralph Scully ◽  
Rajula Elango ◽  
Arvind Panday ◽  
Francis Lach ◽  
Nicholas Willis ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Homologous Recombination ◽  
Replication Fork ◽  
Strand Break ◽  
Replication Forks ◽  
Chromosomal Dna ◽  
Site Specific ◽  
A Site ◽  
Break Induced Replication

Abstract Vertebrate replication forks arrested at an interstrand DNA crosslink (ICL) can engage the Fanconi anemia (FA) pathway of ICL repair. The FANCP product, SLX4, binds the FANCQ/XPF/ERCC4-ERCC1 endonuclease, which incises bidirectionally arrested forks to ‘unhook’ the ICL. The resulting double strand break (DSB) is repaired by homologous recombination (HR). Whether this mechanism operates at replication blocks other than ICLs is unknown. Here, we study the role of mammalian SLX4 in HR triggered by a site-specific, chromosomal DNA-protein replication fork barrier formed by the Escherichia coli-derived Tus/Ter complex. We identify an SLX4-XPF-mediated step that is required for Tus/Ter-induced HR but not for HR induced by a replication-independent DSB. We additionally identify a requirement for SLX4-XPF in DSB-induced ‘long tract’ gene conversion, a replicative HR pathway related to break-induced replication. Our work suggests that Tus/Ter-induced HR recapitulates the incision step of replication-coupled ICL repair, and that the full FA mechanism can process DNA-protein barriers for HR.

scholarly journals Role of DNA repair by (A)BC excinuclease and Ogt alkyltransferase in the final distribution of LacI−d mutations induced by N-butyl-N-nitrosourea in Escherichia coli

Mutagenesis ◽  
1998 ◽  
Vol 13 (5) ◽  
pp. 507-514 ◽  
Author(s):  
Francisco Ferrezuelo ◽  
María-José Prieto-Álamo ◽  
Juan Jurado ◽  
Carmen Pueyo
Keyword(s):  
Escherichia Coli ◽  
Dna Repair

RecBCD enzyme overproduction impairs DNA repair and homologous recombination in Escherichia coli

2005 ◽  
Vol 156 (3) ◽  
pp. 304-311 ◽  
Author(s):  
Damir Đermić ◽  
Edyta Halupecki ◽  
Davor Zahradka ◽  
Mirjana Petranović
Keyword(s):  
Escherichia Coli ◽  
Dna Repair ◽  
Homologous Recombination ◽  
Enzyme Overproduction ◽  
Recbcd Enzyme

scholarly journals Erratum: Homologous recombination in Candida albicans: role of CaRad52p in DNA repair, integration of linear DNA fragments and telomere length

2005 ◽  
Vol 56 (5) ◽  
pp. 1396-1396 ◽  
Author(s):  
Toni Ciudad ◽  
Encarnación Andaluz ◽  
Olga Steinberg-Neifach ◽  
Neal F. Lue ◽  
Neil A. R. Gow ◽  
...  
Keyword(s):  
Dna Repair ◽  
Candida Albicans ◽  
Homologous Recombination ◽  
Telomere Length ◽  
Dna Fragments ◽  
Linear Dna

scholarly journals Mechanisms of Transcription-Replication Collisions in Bacteria

2005 ◽  
Vol 25 (3) ◽  
pp. 888-895 ◽  
Author(s):  
Ekaterina V. Mirkin ◽  
Sergei M. Mirkin
Keyword(s):  
Escherichia Coli ◽  
Direct Contact ◽  
Replication Origin ◽  
Replication Fork ◽  
Mutual Orientation ◽  
Physical Interaction ◽  
Inducible Promoters ◽  
Replication Fork Progression ◽  
Replication Intermediates

ABSTRACT While collisions between replication and transcription in bacteria are deemed inevitable, the fine details of the interplay between the two machineries are poorly understood. In this study, we evaluate the effects of transcription on the replication fork progression in vivo, by using electrophoresis analysis of replication intermediates. Studying Escherichia coli plasmids, which carry constitutive or inducible promoters in different orientations relative to the replication origin, we show that the mutual orientation of the two processes determines their mode of interaction. Replication elongation appears not to be affected by transcription proceeding in the codirectional orientation. Head-on transcription, by contrast, leads to severe inhibition of the replication fork progression. Furthermore, we evaluate the mechanism of this inhibition by limiting the area of direct contact between the two machineries. We observe that replication pausing zones coincide exactly with transcribed DNA segments. We conclude, therefore, that the replication fork is most likely attenuated upon direct physical interaction with the head-on transcription machinery.

scholarly journals Role of the Insulin-Like Growth Factor I/Insulin Receptor Substrate 1 Axis in Rad51 Trafficking and DNA Repair by Homologous Recombination

2003 ◽  
Vol 23 (21) ◽  
pp. 7510-7524 ◽  
Author(s):  
Joanna Trojanek ◽  
Thu Ho ◽  
Luis Del Valle ◽  
Michal Nowicki ◽  
Jin Ying Wang ◽  
...  
Keyword(s):  
Dna Repair ◽  
Growth Factor ◽  
Homologous Recombination ◽  
Insulin Receptor ◽  
Insulin Receptor Substrate ◽  
Insulin Like Growth Factor ◽  
Insulin Receptor Substrate 1 ◽  
Factor I ◽  
Igf I

ABSTRACT The receptor for insulin-like growth factor I (IGF-IR) controls normal and pathological growth of cells. DNA repair pathways represent an unexplored target through which the IGF-IR signaling system might support pathological growth leading to cellular transformation. However, this study demonstrates that IGF-I stimulation supports homologous recombination-directed DNA repair (HRR). This effect involves an interaction between Rad51 and the major IGF-IR signaling molecule, insulin receptor substrate 1 (IRS-1). The binding occurs within the cytoplasm, engages the N-terminal domain of IRS-1, and is attenuated by IGF-I-mediated IRS-1 tyrosine phosphorylation. In the absence of IGF-I stimulation, or if mutated IGF-IR fails to phosphorylate IRS-1, localization of Rad51 to the sites of damaged DNA is diminished. These results point to a direct role of IRS-1 in HRR and suggest a novel role for the IGF-IR/IRS-1 axis in supporting the stability of the genome.

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