RAD52 is required for RNA-templated recombination repair in post-mitotic neurons.

ABSTRACT: It has been long assumed that post-mitotic neurons only utilize the error-prone non-homologous end-joining pathway to repair double-strand breaks (DSBs) associated with oxidative damage to DNA, given the inability of non-replicating neuronal DNA to utilize a sister chromatid template in the less error-prone homologous recombination (HR) repair pathway. However, we and others have found recently that active transcription triggers a replication-independent recombinational repair mechanism in G₀/G₁ phase of the cell cycle. Here we observed that the HR repair protein RAD52 is recruited to sites of DNA DSBs in terminally differentiated, post-mitotic neurons. This recruitment is dependent on the presence of a nascent mRNA generated during active transcription, providing evi

SUBMITTER: Welty S 

PROVIDER: S-EPMC5787811 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature