Role of the BLM helicase in replication fork management.
Genomic DNA is particularly vulnerable to mutation during S-phase when the two strands of parental duplex DNA are separated during the process of semi-conservative DNA replication. Lesions that are normally repaired efficiently in the context of double stranded DNA can cause replication forks to stall or, more dangerously, collapse. Cells from Bloom's syndrome patients, that lack the RecQ helicase BLM, show defects in the response to replicative stress and contain a multitude of chromosomal aberrations, which primarily arise through excessive levels of homologous recombination. Here, recent findings are reviewed that further our understanding of the role that BLM plays in the management of damaged replication forks.
Wu
Leonard
L
Cancer Research UK, University of Oxford, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, United Kingdom. leonard.wu@cancer.org.uk
D000251:Adenosine Triphosphatases / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D001816:Bloom Syndrome / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D004265:DNA Helicases / Q000235:genetics* / Q000378:metabolism; D004261:DNA Replication; D006801:Humans; D053484:RecQ Helicases; D011995:Recombination, Genetic; D012854:Sister Chromatid Exchange
D000251:Adenosine Triphosphatases; C097151:Bloom syndrome protein; D004265:DNA Helicases; D053484:RecQ Helicases