Protection or resection: BOD1L as a novel replication fork protection factor

Research output: Contribution to journalArticle

Colleges, School and Institutes

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. Amongst these, the Fanconi Anemia/homologous recombination pathways are critical for recognising 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 supress 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’.

Details

Original languageEnglish
JournalNucleus (Austin)
Early online date18 Feb 2016
Publication statusE-pub ahead of print - 18 Feb 2016