Rev1 contributes to proper mitochondrial function via the PARP-NAD⁺-SIRT1-PGC1α axis.

ABSTRACT: Nucleic acids, which constitute the genetic material of all organisms, are continuously exposed to endogenous and exogenous damaging agents, representing a significant challenge to genome stability and genome integrity over the life of a cell or organism. Unrepaired DNA lesions, such as single- and double-stranded DNA breaks (SSBs and DSBs), and single-stranded gaps can block progression of the DNA replication fork, causing replicative stress and/or cell cycle arrest. However, translesion synthesis (TLS) DNA polymerases, such as Rev1, have the ability to bypass some DNA lesions, which can circumvent the process leading to replication fork arrest and minimize replicative stress. Here, we show that Rev1-deficiency in mouse embryo fibroblasts or mouse liver tissue is associated with replicati

SUBMITTER: Fakouri NB 

PROVIDER: S-EPMC5624938 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature