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Proteins that are covalently bound to DNA constitute a specific type of DNA lesion known as DNA-protein crosslinks (DPCs). DPCs represent physical obstacles to the progression of DNA replication. If not repaired, DPCs cause stalling of DNA replication forks that consequently leads to DNA double-strand breaks, the most cytotoxic DNA lesion. Although DPCs are common DNA lesions, the mechanism of DPC repair was unclear until now. Recent work unveiled that DPC repair is orchestrated by proteolysis performed by two distinct metalloproteases, SPARTAN in metazoans and Wss1 in yeast. This review summarizes recent discoveries on two proteases in DNA replication-coupled DPC repair and establishes DPC proteolysis repair as a separate DNA repair pathway for genome stability and protection from accelerated aging and cancer.

Original publication

DOI

10.1016/j.tibs.2017.03.005

Type

Journal article

Journal

Trends Biochem Sci

Publication Date

06/2017

Volume

42

Pages

483 - 495

Keywords

DNA replication, DNA–protein crosslink, DNA–protein crosslink proteolysis repair, SPARTAN (DVC1) protease, Wss1 protease, aging, cancer, genome stability, Aging, DNA, DNA Repair, Humans, Neoplasms, Proteins, Proteolysis