WRNing for the right DNA repair pathway choice

Abstract

Premature aging diseases, also called ‘progeroid syndrome’, display signs and features of normal aging in early life, ultimately leading to premature death. Although progeroid syndromes do not perfectly mimic chronological aging they can be excellent model systems to study characteristics of normal aging. Werner syndrome (WS) is one of the rare autosomal recessive progeroid syndromes, characterized by accelerated in vivo/in vitro aging [2]. WRN is suggested to play a central role in maintaining genome stability and rapidly recruits to the DNA damage sites to take part in DNA repair, including base excision DNA repair (BER), classical/alternative non-homologous end joining (NHEJ), homologous recombination (HR), and replication re-start after DNA damage.