Open Access Highly Accessed Review

Human single-stranded DNA binding proteins are essential for maintaining genomic stability

Nicholas W Ashton1, Emma Bolderson1, Liza Cubeddu2, Kenneth J O’Byrne1 and Derek J Richard1*

Author Affiliations

1 Genome Stability Laboratory, Cancer and Ageing Research Program, Institute of Health and Biomedical Innovation, Translational Research Institute, Queensland University of Technology, Woolloongabba, Queensland, 4102, Australia

2 School of Science and Health, University of Western Sydney, Sydney, Locked Bag 1797, Penrith, NSW, 2751, Australia

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BMC Molecular Biology 2013, 14:9  doi:10.1186/1471-2199-14-9

Published: 1 April 2013


The double-stranded conformation of cellular DNA is a central aspect of DNA stabilisation and protection. The helix preserves the genetic code against chemical and enzymatic degradation, metabolic activation, and formation of secondary structures. However, there are various instances where single-stranded DNA is exposed, such as during replication or transcription, in the synthesis of chromosome ends, and following DNA damage. In these instances, single-stranded DNA binding proteins are essential for the sequestration and processing of single-stranded DNA. In order to bind single-stranded DNA, these proteins utilise a characteristic and evolutionary conserved single-stranded DNA-binding domain, the oligonucleotide/oligosaccharide-binding (OB)-fold. In the current review we discuss a subset of these proteins involved in the direct maintenance of genomic stability, an important cellular process in the conservation of cellular viability and prevention of malignant transformation. We discuss the central roles of single-stranded DNA binding proteins from the OB-fold domain family in DNA replication, the restart of stalled replication forks, DNA damage repair, cell cycle-checkpoint activation, and telomere maintenance.

Single-stranded DNA binding proteins (SSBs); Oligonucleotide/oligosaccharide binding (OB)-fold; Double-strand DNA break (DSB) repair; Homology-directed repair (HDR); Translesion synthesis; Nucleotide excision repair (NER); Replication fork restart; Cell cycle checkpoint activation; Telomere maintenance