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. 2019 Dec 12;10(1):5671.
doi: 10.1038/s41467-019-13610-7.

A model of DNA damage response activation at stalled replication forks by SPRTN

Christopher Bruhn  1 , Marco Foiani  2   3
Affiliations

A model of DNA damage response activation at stalled replication forks by SPRTN

Christopher Bruhn et al. Nat Commun. .

Abstract

The process of DNA replication is threatened by many factors, including DNA lesions, and machineries acting as obstacles. Here we discuss and speculate on a recently proposed mechanism of DNA damage response activation in response to lesions that challenge the progression of DNA replication forks.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. A model for DPC-induced Chk1 activation during replication.
DPCs can induce fork stalling and topological stress, leading to activation of the SPRTN-CHK1 fork protection regulatory loop. Occasionally, DPCs can induce un-programmed termination sites where adjacent replicons converge without fusing, thus generating topological stress and preventing the completion of replication. Under these circumstances the SPRTN-CHK1 axis inhibits cell cycle progression to avoid segregation of partially replicated chromosomes.
See this image and copyright information in PMC

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