title: Protection or resection: BOD1L as a novel replication fork protection factor.
abstract: Replication stress, defined as the slowing or stalling of cellular DNA replication forks, represents a serious threat to genome stability. Numerous cellular pathways protect against replication stress and maintain genomic integrity. Among these, the Fanconi Anemia/homologous recombination pathways are critical for recognizing and repairing stalled replication forks. Members of these pathways play a vital role in protecting damaged forks from uncontrolled attack from cellular nucleases, which would otherwise render these irreparable. Recent studies have begun to shed light on the protective factors necessary to suppress nucleolytic over-processing of nascent DNA, and on the different cellular nucleases involved. Here, we review our recent identification of a novel fork protection factor, BOD1L, and discuss its role in preventing the processing of stalled replication forks within the context of current knowledge of the replication fork 'protectosome'.
authors.affiliation: a Institute of Cancer and Genomic Studies , University of Birmingham , Birmingham , UK.
authors.forename: Martin R
authors.initials: MR
authors.lastname: Higgs
authors.affiliation: a Institute of Cancer and Genomic Studies , University of Birmingham , Birmingham , UK.
authors.forename: Grant S
authors.initials: GS
authors.lastname: Stewart
mesh_terms: D000818:Animals; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D004247:DNA / Q000096:biosynthesis* / Q000235:genetics; D004261:DNA Replication / Q000502:physiology*; D042822:Genomic Instability / Q000502:physiology*; D006801:Humans
chemical_list: C524692:Bod1 protein, human; D018797:Cell Cycle Proteins; D004247:DNA
keywords: BOD1L; RAD51; fanconi anaemia; homologous recombination; nascent strand degradation; replication stress