Role for BLM in replication-fork restart and suppression of origin firing after replicative stress
SL Davies, PS North, ID Hickson - Nature structural & molecular biology, 2007 - nature.com
SL Davies, PS North, ID Hickson
Nature structural & molecular biology, 2007•nature.comMutations in BLM give rise to Bloom's syndrome, a genetic disorder associated with cancer
predisposition and chromosomal instability. Using a dual-labeling system in isolated
chromosome fibers, we show that the BLM protein is required for two aspects of the cellular
response to replicative stress: efficient replication-fork restart and suppression of new origin
firing. These functions require the helicase activity of BLM and the Thr99 residue targeted by
stress-activated kinases.
predisposition and chromosomal instability. Using a dual-labeling system in isolated
chromosome fibers, we show that the BLM protein is required for two aspects of the cellular
response to replicative stress: efficient replication-fork restart and suppression of new origin
firing. These functions require the helicase activity of BLM and the Thr99 residue targeted by
stress-activated kinases.
Abstract
Mutations in BLM give rise to Bloom's syndrome, a genetic disorder associated with cancer predisposition and chromosomal instability. Using a dual-labeling system in isolated chromosome fibers, we show that the BLM protein is required for two aspects of the cellular response to replicative stress: efficient replication-fork restart and suppression of new origin firing. These functions require the helicase activity of BLM and the Thr99 residue targeted by stress-activated kinases.
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