title: Role for BLM in replication-fork restart and suppression of origin firing after replicative stress.
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.
authors.affiliation: Cancer Research UK Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK.
authors.forename: Sally L
authors.initials: SL
authors.lastname: Davies
authors.forename: Phillip S
authors.initials: PS
authors.lastname: North
authors.forename: Ian D
authors.initials: ID
authors.lastname: Hickson
mesh_terms: D000251:Adenosine Triphosphatases / Q000235:genetics / Q000502:physiology*; D002478:Cells, Cultured; D004265:DNA Helicases / Q000235:genetics / Q000502:physiology*; D004261:DNA Replication / Q000187:drug effects; D006801:Humans; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D053484:RecQ Helicases; D018741:Replication Origin; D013912:Threonine / Q000378:metabolism
chemical_list: D013912:Threonine; D017346:Protein Serine-Threonine Kinases; D000251:Adenosine Triphosphatases; C097151:Bloom syndrome protein; D004265:DNA Helicases; D053484:RecQ Helicases