RTEL1: an essential helicase for telomere maintenance and the regulation of homologous recombination

Abstract

Telomere maintenance and DNA repair are crucial processes that protect the genome against instability. RTEL1, an essential iron–sulfur cluster-containing helicase, is a dominant factor that controls telomere length in mice and is required for telomere integrity. In addition, RTEL1 promotes synthesis-dependent strand annealing to direct DNA double-strand breaks into non-crossover outcomes during mitotic repair and in meiosis. Here, we review the role of RTEL1 in telomere maintenance and homologous recombination and discuss models linking RTEL1’s enzymatic activity to its function in telomere maintenance and DNA repair.

The RTEL1 rs6010620 Polymorphism and Glioma Risk: a Meta-analysis Based on 12 Case-control Studies

“…Previous studies proposed that RTEL1 maintains genomic stability by suppressing homologous recombination (Barber et al, 2008;Uringa et al, 2012) and implements a second level of meiotic crossover control by promoting non-crossovers (Mirabello et al, 2010;Youds et al, 2010). A recent review indicated that RTEL1 is an essential helicase for telomere maintenance and regulation of homologous recombination (Adelman and Boulton, 2010;Uringa et al, 2011). RTEL1 is overexpressed in human gastrointestinal tract tumors (Bai et al, 2000), and RTEL1 gene polymorphisms are associated with glioblastoma survival (Liu et al, 2010).…”

Novel Function of the Fanconi Anemia Group J or RECQ1 Helicase to Disrupt Protein-DNA Complexes in a Replication Protein A-stimulated Manner

“…WRN, BLM, and RTEL) help to preserve telomere stability by unwinding T-loops and G4 DNA; alternatively, certain helicases (e.g. PIF1) catalytically displace telomerase from DNA to facilitate replication and DNA repair (17)(18)(19). Understanding how the catalytic functions of DNA helicases are regulated remains an important question in telomere biology.…”

RTEL1, une hélicase de l’ADN essentielle à la stabilité du génome

“…La réplication des extrémi-tés des chromosomes eucaryotes est incomplète (end replication problem) et conduit à un raccourcissement SYNTHÈSE REVUES (aussi appelée CHL1 ou CHLR1, et dont la déficience est responsable du syndrome Warsaw breakage) et FANCJ (dont la déficience est responsable de l'anémie de Fanconi) appartient à une sous-famille d'hélicases d'ADN qui contiennent un domaine fer-soufre (Fe-S). RTEL1 requiert l'activité du facteur d'assemblage MMS19 pour le transfert des ions Fe-S, qui lui permet d'être correctement structurée [22][23][24]. La plupart des informations fonctionnelles dont nous disposons pour RTEL1 proviennent d'études réalisées chez le nématode Caenorhabditis elegans et la souris.…”