Abstract
DNA replication can encounter blocking obstacles, leading to replication stress and genome instability. There are several mechanisms for evading this blockade. One mechanism consists of repriming ahead of the obstacles, creating a new starting point; in humans, PrimPol is responsible for carrying out this task. PrimPol is a primase that operates in both the nucleus and mitochondria. In contrast with conventional primases, PrimPol is a DNA primase able to initiate DNA synthesis de novo using deoxynucleotides, discriminating against ribonucleotides. In vitro, PrimPol can act as a DNA primase, elongating primers that PrimPol itself sythesizes, or as translesion synthesis (TLS) DNA polymerase, elongating pre-existing primers across lesions. However, the lack of evidence for PrimPol polymerase activity in vivo suggests that PrimPol only acts as a DNA primase. Here, we provide a comprehensive review of human PrimPol covering its biochemical properties and structure, in vivo function and regulation, and the processes that take place to fill the gap-containing lesion that PrimPol leaves behind. Finally, we explore the available data on human PrimPol expression in different tissues in physiological conditions and its role in cancer.
Highlights
PrimPol, a New Enzyme Working on DNA ReplicationIn human cells, DNA replication is initiated by the primosome [1,2]
In vitro abilities of PrimPol, primase discovered [81]: PrimPol is able to directly read 8oxodG when it catalyzes the it is probable that in vivo PrimPol uses its translesion synthesis (TLS) abilities to be proficient as a DNA primase synthesis of de novo primer (Figure 3A), or realigning the primer that PrimPol itself is catinvolved in restarting stalled replication forks
The discovery of PrimPol, the first DNA primase discovered in human cells, was a breakthrough in the DNA replication field [12]
Summary
Replication carries out this task in BRCA1/2 cells, a scenario involving the accumulation rep of DNA due to PrimPol-mediated repriming (Figure 9 top right panel). DNA replication is initiated by ribonucleotide Academic with the regulatory subunit, during the formation of the full primer and Editor: Anthony J. [6,7] establishes that to elongate the small RNA primers dNTPs, ma model of DNAtional replication the leading-strand requires thewith priming publication under the terms and connucleotides with a 5′polymerase portion of RNA and a 3′ portio ditions of the Creative Commons Atevent for the primosome and elongation for the replicative. Pol δ copy the donor template, and the single strand returns to its starting site to continue the synthesis ahead of the lesion by Pol ε. (Top right panel): translesion synthesis (TLS)
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