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PARP is activated at stalled forks to mediate Mre11‐dependent replication restart and recombination
If replication forks are perturbed, a multifaceted response including several DNA repair and cell cycle checkpoint pathways is activated to ensure faithful DNA replication. Here, we show thatExpand
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  • Open Access
Modulation of RNA Polymerase by (p)ppGpp Reveals a RecG-Dependent Mechanism for Replication Fork Progression
We have discovered a correlation between the ability of Escherichia coli cells to survive damage to DNA and their ability to modulate RNA polymerase via the stringent response regulators, (p)ppGpp.Expand
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Recombinational repair and restart of damaged replication forks
Genome duplication necessarily involves the replication of imperfect DNA templates and, if left to their own devices, replication complexes regularly run into problems. The details of how cellsExpand
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PriA helicase and SSB interact physically and functionally.
PriA helicase is the major DNA replication restart initiator in Escherichia coli and acts to reload the replicative helicase DnaB back onto the chromosome at repaired replication forks and D-loopsExpand
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  • Open Access
Rep Provides a Second Motor at the Replisome to Promote Duplication of Protein-Bound DNA
Summary Nucleoprotein complexes present challenges to genome stability by acting as potent blocks to replication. One attractive model of how such conflicts are resolved is direct targeting ofExpand
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Replication fork reversal and the maintenance of genome stability
The progress of replication forks is often threatened in vivo, both by DNA damage and by proteins bound to the template. Blocked forks must somehow be restarted, and the original blockage cleared, inExpand
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  • Open Access
The DNA replication protein PriA and the recombination protein RecG bind D-loops.
The PriA protein of Escherichia coli provides a vital link between recombination and DNA replication. To establish the molecular basis for this link, we investigated the ability of PriA to target DNAExpand
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Genome stability and the processing of damaged replication forks by RecG.
Chromosomal duplication faces many blocks to replication fork progression that could destabilize the genome and prove fatal if not overcome. Overcoming such blocks requires interplay between DNAExpand
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Rescue of stalled replication forks by RecG: Simultaneous translocation on the leading and lagging strand templates supports an active DNA unwinding model of fork reversal and Holliday junction
Modification of damaged replication forks is emerging as a crucial factor for efficient chromosomal duplication and the avoidance of genetic instability. The RecG helicase of Escherichia coli, whichExpand
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  • Open Access
Direct rescue of stalled DNA replication forks via the combined action of PriA and RecG helicase activities.
The PriA protein of Escherichia coli plays a key role in the rescue of replication forks stalled on the template DNA. One attractive model of rescue relies on homologous recombination to establish aExpand
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