Genome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton BN1 9RQ, UK.
Mol Cell. 2013 Nov 21;52(4):566-73. doi: 10.1016/j.molcel.2013.10.035.
DNA damage can stall the DNA replication machinery, leading to genomic instability. Thus, numerous mechanisms exist to complete genome duplication in the absence of a pristine DNA template, but identification of the enzymes involved remains incomplete. Here, we establish that Primase-Polymerase (PrimPol; CCDC111), an archaeal-eukaryotic primase (AEP) in eukaryotic cells, is involved in chromosomal DNA replication. PrimPol is required for replication fork progression on ultraviolet (UV) light-damaged DNA templates, possibly mediated by its ability to catalyze translesion synthesis (TLS) of these lesions. This PrimPol UV lesion bypass pathway is not epistatic with the Pol η-dependent pathway and, as a consequence, protects xeroderma pigmentosum variant (XP-V) patient cells from UV-induced cytotoxicity. In addition, we establish that PrimPol is also required for efficient replication fork progression during an unperturbed S phase. These and other findings indicate that PrimPol is an important player in replication fork progression in eukaryotic cells.
DNA 损伤可使 DNA 复制机制停滞,导致基因组不稳定。因此,尽管不存在原始 DNA 模板,仍存在许多机制来完成基因组的复制,但涉及的酶的鉴定仍不完整。在这里,我们确定了原核生物-真核生物聚合酶(PrimPol;CCDC111),真核细胞中的一种古细菌-真核生物聚合酶(AEP),参与了染色体 DNA 的复制。PrimPol 对于紫外线(UV)光损伤 DNA 模板上的复制叉推进是必需的,可能是通过其催化这些损伤的跨损伤合成(TLS)的能力介导的。这种 PrimPol UV 损伤绕过途径与 Pol η 依赖性途径没有上位性,因此,保护着色性干皮病变异型(XP-V)患者细胞免受 UV 诱导的细胞毒性。此外,我们确定 PrimPol 对于在未受干扰的 S 期内有效复制叉推进也是必需的。这些和其他发现表明 PrimPol 是真核细胞中复制叉推进的重要参与者。