Translesion synthesis by Y family DNA polymerases bypasses lesions on DNA template

Stable Identifier
R-HSA-110313
Type
Pathway
Species
Homo sapiens
Compartment
Locations in the PathwayBrowser
General
SVG |   | PPTX  | SBGN
Click the image above or here to open this pathway in the Pathway Browser

Ubiquitous environmental and endogenous genotoxic agents cause DNA lesions that can interfere with normal DNA metabolism including DNA replication, eventually resulting in mutations that lead to carcinogenesis and/or cell death. Cells possess repair mechanisms like nucleotide excision and base excision repair pathways to maintain the integrity of the genome. However, some types of lesions are repaired very inefficiently and others may not be recognized and repaired before the lesion-containing DNA undergoes DNA replication. To prevent acute cell death through arrested DNA replication at unrepaired lesions, cells have a mechanism, referred to as translesion synthesis (TLS), which allows DNA synthesis to proceed past lesions. TLS depends on the Y family of DNA polymerases (Lindahl and Wood 1999, Masutani et al. 2000, Yang 2014).

Literature References
PubMed ID Title Journal Year
24716551 An overview of Y-Family DNA polymerases and a case study of human DNA polymerase ?

Yang, W

Biochemistry 2014
10583946 Quality control by DNA repair

Lindahl, T, Wood, RD

Science 1999
10856253 Mechanisms of accurate translesion synthesis by human DNA polymerase eta.

Masutani, C, Kusumoto, R, Iwai, S, Hanaoka, F

EMBO J 2000
Participants
Participant Of
Event Information
Go Biological Process
Orthologous Events
Authored
Reviewed
Created