Rad18-dependent SUMOylation of human specialized DNA polymerase eta is required to prevent under-replicated DNA

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Abstract

Translesion polymerase eta {(polη)} was characterized for its ability to replicate ultraviolet-induced {DNA} lesions that stall replicative polymerases, a process promoted by Rad18-dependent {PCNA} mono-ubiquitination. Recent findings have shown that {polη} also acts at intrinsically difficult to replicate sequences. However, the molecular mechanisms that regulate its access to these loci remain elusive. Here, we uncover that {polη} travels with replication forks during unchallenged S phase and this requires its {SUMOylation} on K163. Abrogation of {polη} {SUMOylation} results in replication defects in response to mild replication stress, leading to chromosome fragments in mitosis and damage transmission to daughter cells. Rad18 plays a pivotal role, independently of its ubiquitin ligase activity, acting as a molecular bridge between {polη} and the {PIAS1} {SUMO} ligase to promote {polη} {SUMOylation.} Our results provide the first evidence that {SUMOylation} represents a new way to target {polη} to replication forks, independent of the Rad18-mediated {PCNA} ubiquitination, thereby preventing under-replicated {DNA.}

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Despras, E., Sittewelle, M., Pouvelle, C., Delrieu, N., Cordonnier, A. M., & Kannouche, P. L. (2016). Rad18-dependent SUMOylation of human specialized DNA polymerase eta is required to prevent under-replicated DNA. Nature Communications, 7. https://doi.org/10.1038/ncomms13326

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