The contribution of dormant origins to genome stability: from cell biology to human genetics

Robert C. Alver; Gaganmeet Singh Chadha; J. Julian Blow

doi:10.1016/j.dnarep.2014.03.012

The contribution of dormant origins to genome stability: from cell biology to human genetics

Robert C. Alver, Gaganmeet Singh Chadha, J. Julian Blow

Research output: Contribution to journal › Article › peer-review

83 Citations (Scopus)

Abstract

The ability of a eukaryotic cell to precisely and accurately replicate its DNA is crucial to maintain genome stability. Here we describe our current understanding of the process by which origins are licensed for DNA replication and review recent work suggesting that fork stalling has exerted a strong selective pressure on the positioning of licensed origins. In light of this, we discuss the complex and disparate phenotypes observed in mouse models and humans patients that arise due to defects in replication licensing proteins.

Original language	English
Pages (from-to)	182-189
Number of pages	8
Journal	DNA Repair
Volume	19
DOIs	https://doi.org/10.1016/j.dnarep.2014.03.012
Publication status	Published - Jul 2014

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10.1016/j.dnarep.2014.03.012Licence: CC BY

Cite this

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title = "The contribution of dormant origins to genome stability: from cell biology to human genetics",

abstract = "The ability of a eukaryotic cell to precisely and accurately replicate its DNA is crucial to maintain genome stability. Here we describe our current understanding of the process by which origins are licensed for DNA replication and review recent work suggesting that fork stalling has exerted a strong selective pressure on the positioning of licensed origins. In light of this, we discuss the complex and disparate phenotypes observed in mouse models and humans patients that arise due to defects in replication licensing proteins.",

author = "Alver, {Robert C.} and Chadha, {Gaganmeet Singh} and Blow, {J. Julian}",

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AB - The ability of a eukaryotic cell to precisely and accurately replicate its DNA is crucial to maintain genome stability. Here we describe our current understanding of the process by which origins are licensed for DNA replication and review recent work suggesting that fork stalling has exerted a strong selective pressure on the positioning of licensed origins. In light of this, we discuss the complex and disparate phenotypes observed in mouse models and humans patients that arise due to defects in replication licensing proteins.

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DO - 10.1016/j.dnarep.2014.03.012

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