Creation and resolution of non-B-DNA structural impediments during replication
Open Access
- 28 September 2022
- journal article
- review article
- Published by Taylor & Francis in Critical Reviews in Biochemistry and Molecular Biology
- Vol. 57 (4) , 412-442
Abstract
During replication, folding of the DNA template into non-B-form secondary structures provides one of the most abundant impediments to the smooth progression of the replisome. The core replisome collaborates with multiple accessory factors to ensure timely and accurate duplication of the genome and epigenome. Here, we discuss the forces that drive non-B structure formation and the evidence that secondary structures are a significant and frequent source of replication stress that must be actively countered. Taking advantage of recent advances in the molecular and structural biology of the yeast and human replisomes, we examine how structures form and how they may be sensed and resolved during replication.Keywords
Funding Information
- Darwin Trust of Edinburgh
This publication has 339 references indexed in Scilit:
- Role of DNA Polymerases in Repeat-Mediated Genome InstabilityCell Reports, 2012
- Selective Bypass of a Lagging Strand Roadblock by the Eukaryotic Replicative DNA HelicaseCell, 2011
- Human Senataxin Resolves RNA/DNA Hybrids Formed at Transcriptional Pause Sites to Promote Xrn2-Dependent TerminationMolecular Cell, 2011
- Epigenetic Instability due to Defective Replication of Structured DNAMolecular Cell, 2010
- Human DHX9 Helicase Unwinds Triple-Helical DNA StructuresBiochemistry, 2010
- Large-Scale Expansions of Friedreich's Ataxia GAA Repeats in YeastMolecular Cell, 2009
- Mammalian Telomeres Resemble Fragile Sites and Require TRF1 for Efficient ReplicationCell, 2009
- Role of TLS DNA polymerases eta and kappa in processing naturally occurring structured DNA in human cellsMolecular Carcinogenesis, 2008
- The Mcm2-7 Complex Has In Vitro Helicase ActivityMolecular Cell, 2008
- Activation of Ubiquitin-Dependent DNA Damage Bypass Is Mediated by Replication Protein AMolecular Cell, 2008