The importance of repairing stalled replication forks

Article Abstract:

The clear prevalence of replication fork demise and reactivation may demand a readjustment of the commonly quoted rate of replication fork propagation of 1,000 nucleotides per second. This rate has been based on the time needed for completion of one round of chromosomal replication. Research in this area has focused on the nonmutagenic pathways for replication fork reactivation and the enzymes involved in them. It is clear that replication can be halted by DNA damage, but little is known about the molecular events connected with the demise of a replication fork.

DNA repair, Chromosome replication

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Purposeful mutations

Article Abstract:

The SOS mutagenic response may a cell's final attempt to survive when DNA damage outstrips its capacity for repair. UmuD and UmuC proteins are induced in the SOS response to DNA damage. Tang and colleagues have purified an intact, native UmuD'(sub2)C complex. They undertook replication using a primed bacteriophage M13 DNA template incorporating a single, synthetic, abasic lesion. Synthesis by pol III was found to be entirely blocked one base before the lesion, and lesion bypass required mutasomal proteins.

DNA, Mutagenesis

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Replication fork reactivation downstream of a blocked nascent leading strand

Article Abstract:

A study demonstrates 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 DnaG primase of both the leading and lagging strands. The results provide a mechanism for damage bypass during fork reactivation, demonstrating how daughter-strand gaps are generated opposite leading-strand lesions during the replication of ultraviolet-light irradiated DNA.

Science & research, Gene mutations, Gene mutation, DNA replication

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