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Comment
. 2016 Feb 4;12(2):e1005742.
doi: 10.1371/journal.pgen.1005742. eCollection 2016 Feb.

EEPD1: Breaking and Rescuing the Replication Fork

Yilun Liu  1
Affiliations
Comment

EEPD1: Breaking and Rescuing the Replication Fork

Yilun Liu. PLoS Genet. .
No abstract available

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Conflict of interest statement

The author has declared that no competing interests exist.

Figures

Fig 1
Fig 1. Potential pathways to repair and restart a stalled replication fork.
Parental DNA strands (blue) and newly synthesized DNA strands (red) form a stalled fork due to the presence of DNA damage or replication blockage (brown triangle). Left: In the classical model, ssDNA at a stalled replication fork is bound by replication protein A (RPA), which recruits ataxia telangiectasia and Rad3-related protein (ATR) to activate the DNA damage response. ATR-dependent DNA damage response stabilizes the stalled replication fork, whose damage or blockage is repaired by DNA lesion bypass, direct damage removal, or template-switching via fork regression. Right: The EEPD1-Exo1-BLM) constitutive complex may provide an alternative pathway by nicking the 5′ single-stranded region of the stalled strand to generate a DNA double-stranded break, which is resected to form a 3′ single-stranded overhang to initiate homologous recombination (HR).
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