ReviewProceedings of the National Academy of Sciences of the United States of America2001
The tight linkage between DNA replication and double-strand break repair in bacteriophage T4.
Review in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- Mechanisms of Type I-E and I-F CRISPR-Cas Systems inEcoSal Plus · 2019Review
- Unexpected evolutionary benefit to phages imparted by bacterial CRISPR-Cas9.Science advances · 2018Article
- Break-induced DNA replication.Cold Spring Harbor perspectives in biology · 2013Review
- Coordination and processing of DNA ends during double-strand break repair: the role of the bacteriophage T4 Mre11/Rad50 (MR) complex.Genetics · 2013Article
- Interaction of T4 UvsW helicase and single-stranded DNA binding protein gp32 through its carboxy-terminal acidic tail.Journal of molecular biology · 2013Article
- Biochemical characterization of bacteriophage T4 Mre11-Rad50 complex.The Journal of biological chemistry · 2011Article
- Initiation of bacteriophage T4 DNA replication and replication fork dynamics: a review in the Virology Journal series on bacteriophage T4 and its relatives.Virology journal · 2010Review
- The pol3-t hyperrecombination phenotype and DNA damage-induced recombination in Saccharomyces cerevisiae is RAD50 dependent.Journal of biomedicine & biotechnology · 2009Article
- Defective break-induced replication leads to half-crossovers in Saccharomyces cerevisiae.Genetics · 2008Article
- The phage T4 protein UvsW drives Holliday junction branch migration.The Journal of biological chemistry · 2007Article
- Inhibition of mutation and combating the evolution of antibiotic resistance.PLoS biology · 2005Article
- Gyrase inhibitors and thymine starvation disrupt the normal pattern of plasmid RK2 localization in Escherichia coli.Journal of bacteriology · 2005Article
- MRE11/RAD50/NBS1: complex activities.Chromosoma · 2004Review
- Role of DNA replication proteins in double-strand break-induced recombination in Saccharomyces cerevisiae.Molecular and cellular biology · 2004Article
- Repair system for noncanonical purines in Escherichia coli.Journal of bacteriology · 2003Article
- Article
- Cancer predisposition and hematopoietic failure in Rad50(S/S) mice.Genes & development · 2002Article
- DNA replication meets genetic exchange: chromosomal damage and its repair by homologous recombination.Proceedings of the National Academy of Sciences of the United States of America · 2001Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Double-strand break (DSB) repair and DNA replication are tightly linked in the life cycle of bacteriophage T4. Indeed, the major mode of phage DNA replication depends on recombination proteins and can be stimulated by DSBs. DSB-stimulated DNA replication is dramatically demonstrated when T4 infects cells carrying two plasmids that share homology. A DSB on one plasmid triggered extensive replication of the second plasmid, providing a useful model for T4 recombination-dependent replication (RDR). This system also provides a view of DSB repair in T4-infected cells and revealed that the DSB repair products had been replicated in their entirety by the T4 replication machinery. We analyzed the detailed structure of these products, which do not fit the simple predictions of any of three models for DSB repair. We also present evidence that the T4 RDR system functions to restart stalled or inactivated replication forks. First, we review experiments involving antitumor drug-stabilized topoisomerase cleavage complexes. The results suggest that forks blocked at cleavage complexes are resolved by recombinational repair, likely involving RDR. Second, we show here that the presence of a T4 replication origin on one plasmid substantially stimulated recombination events between it and a homologous second plasmid that did not contain a T4 origin. Furthermore, replication of the second plasmid was increased when the first plasmid contained the T4 origin. Our interpretation is that origin-initiated forks become inactivated at some frequency during replication of the first plasmid and are then restarted via RDR on the second plasmid.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.