Fork Reversal and ssDNA Accumulation at Stalled Replication Forks Owing to Checkpoint Defects

By J. Sogo, Massimo Lopes, M. Foiani. Science, 2002

873 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/8c45b2498dc8d56a395c0de6c4b1418e8c949c69

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

Citations in the corpus

Maintaining genome stability at the replication fork (2010, background): “The ATR (Mec1 in yeast) pathway is activated by stalled RFs with exposed ssDNA regions coated with replication protein A (RPA), and they have a central role in promoting RF stabilization and DNA repai”
S-phase checkpoint proteins Tof1 and Mrc1 form a stable replication-pausing complex (2003, background): “Thus, checkpoint factors are thought to act not only to arrest replication but also to maintain a stable replication complex at replication fork”
DNA end resection, homologous recombination and DNA damage checkpoint activation require CDK1 (2004, background): “, during which ssDNA intermediates arise at stalled replication fork”
Functional uncoupling of MCM helicase and DNA polymerase activities activates the ATR-dependent checkpoint. (2005, background): “A study in yeast shows only a modest increase in the amount of ssDNA generated in response to HU (Sogo et al. 2002).”
Genome instability: a mechanistic view of its causes and consequences (2008, background): “Nevertheless, under replication stress, which is caused by a replication inhibition and/or S-phase checkpoint inactivation ( Box 1 ), RFs can collapse causing replisome disassembly, ssDNA gaps and DNA break”
Surviving the breakup: the DNA damage checkpoint. (2006, background): “ssDNA is a useful common checkpoint signal as it is formed during nucleotide and base excision repair, and at stalled replication forks (16, 132).”
Continued primer synthesis at stalled replication forks contributes to checkpoint activation (2010, background): “When forks stall at lesions that do not block helicase progression, these activities functionally uncouple, allowing continued unwinding, ssDNA accumulation, and checkpoint activation (Walter and Newport, 2000; Sogo et al., 2002; Pacek and Walter, 2004; Byun et al., 2005; Liu et al., 2007).”
DNA interstrand crosslink repair and cancer (2011, neutral): “, and chicken foot structures have been shown to exist in vivo and in vitro”