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Merck

EXO1 resection at G-quadruplex structures facilitates resolution and replication.

Nucleic acids research (2020-04-02)
Susanna Stroik, Kevin Kurtz, Kevin Lin, Sergey Karachenets, Chad L Myers, Anja-Katrin Bielinsky, Eric A Hendrickson
ABSTRACT

G-quadruplexes represent unique roadblocks to DNA replication, which tends to stall at these secondary structures. Although G-quadruplexes can be found throughout the genome, telomeres, due to their G-richness, are particularly predisposed to forming these structures and thus represent difficult-to-replicate regions. Here, we demonstrate that exonuclease 1 (EXO1) plays a key role in the resolution of, and replication through, telomeric G-quadruplexes. When replication forks encounter G-quadruplexes, EXO1 resects the nascent DNA proximal to these structures to facilitate fork progression and faithful replication. In the absence of EXO1, forks accumulate at stabilized G-quadruplexes and ultimately collapse. These collapsed forks are preferentially repaired via error-prone end joining as depletion of EXO1 diverts repair away from error-free homology-dependent repair. Such aberrant repair leads to increased genomic instability, which is exacerbated at chromosome termini in the form of dysfunction and telomere loss.

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Sigma-Aldrich
Anticorpo anti-strutture G-quadruplex, clone BG4, clone BG4, from Escherichia coli
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Anticorpo anti-DNA G-quadruplex (G4), clone 1H6, clone 1H6, from mouse
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