PMID:16452972
| Citation |
Heller, RC and Marians, KJ (2006) Replication fork reactivation downstream of a blocked nascent leading strand. Nature 439:557-62 |
|---|---|
| Abstract |
Unrepaired lesions in the DNA template pose a threat to accurate replication. Several pathways exist in Escherichia coli to reactivate a blocked replication fork. The process of recombination-dependent restart of broken forks is well understood, but the consequence of replication through strand-specific lesions is less well known. Here we show that replication can be restarted and leading-strand synthesis re-initiated downstream of an unrepaired block to leading-strand progression, even when the 3'-OH of the nascent leading strand is unavailable. We demonstrate that the loading by a replication restart system of a single hexamer of the replication fork helicase, DnaB, on the lagging-strand template is sufficient to coordinate priming by the DnaG primase of both the leading and lagging strands. These observations provide a mechanism for damage bypass during fork reactivation, demonstrate how daughter-strand gaps are generated opposite leading-strand lesions during the replication of ultraviolet-light-irradiated DNA, and help to explain the remarkable speed at which even a heavily damaged DNA template is replicated. |
| Links |
PubMed Online version:10.1038/nature04329 |
| Keywords |
Adenosine Triphosphatases/metabolism; Bacterial Proteins/metabolism; Biotin/metabolism; DNA/biosynthesis; DNA/metabolism; DNA Helicases/metabolism; DNA Primase/metabolism; DNA Repair; DNA Replication/physiology; DnaB Helicases; Endodeoxyribonucleases/metabolism; Escherichia coli/enzymology; Escherichia coli/genetics; Escherichia coli Proteins/metabolism; Exodeoxyribonucleases/metabolism; Models, Genetic; Templates, Genetic |
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