Affordable Access

Access to the full text

Lesion Bypass and the Reactivation of Stalled Replication Forks

Authors
  • Marians, Kenneth J.
Type
Published Article
Journal
Annual Review of Biochemistry
Publisher
Annual Reviews
Publication Date
Jun 20, 2018
Volume
87
Pages
217–238
Identifiers
DOI: 10.1146/annurev-biochem-062917-011921
Source
Annual Reviews
Keywords
License
Yellow

Abstract

Accurate transmission of the genetic information requires complete duplication of the chromosomal DNA each cell division cycle. However, the idea that replication forks would form at origins of DNA replication and proceed without impairment to copy the chromosomes has proven naive. It is now clear that replication forks stall frequently as a result of encounters between the replication machinery and template damage, slow-moving or paused transcription complexes, unrelieved positive superhelical tension, covalent protein–DNA complexes, and as a result of cellular stress responses. These stalled forks are a major source of genome instability. The cell has developed many strategies for ensuring that these obstructions to DNA replication do not result in loss of genetic information, including DNA damage tolerance mechanisms such as lesion skipping, whereby the replisome jumps the lesion and continues downstream; template switching both behind template damage and at the stalled fork; and the error-prone pathway of translesion synthesis.

Report this publication

Statistics

Seen <100 times