Lesion Bypass and the Reactivation of Stalled Replication Forks.
Annu Rev Biochem
; 87: 217-238, 2018 06 20.
Article
en En
| MEDLINE
| ID: mdl-29298091
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.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Daño del ADN
/
Reparación del ADN
/
Replicación del ADN
Límite:
Humans
Idioma:
En
Revista:
Annu Rev Biochem
Año:
2018
Tipo del documento:
Article