Construction of a vector containing a site-specific DNA double-strand break with 3-phosphoglycolate termini and analysis of the products of end-joining in CV-1 cells '

1996 ◽  
Vol 70 (6) ◽  
pp. 623-636 ◽  
Author(s):  
R. A. O. BENNETT, XIAO-YAN GU and L. F
Keyword(s):  
Strand Break ◽  
Double Strand Break ◽  
End Joining ◽  
Site Specific ◽  
Dna Double Strand Break ◽  
A Site

scholarly journals Molecular Analysis of Base Damage Clustering Associated with a Site-Specific Radiation-Induced DNA Double-Strand Break

2006 ◽  
Vol 166 (5) ◽  
pp. 767-781 ◽  
Author(s):  
Kamal Datta ◽  
Pawel Jaruga ◽  
Miral Dizdaroglu ◽  
Ronald D. Neumann ◽  
Thomas A. Winters
Keyword(s):  
Molecular Analysis ◽  
Strand Break ◽  
Double Strand Break ◽  
Base Damage ◽  
Site Specific ◽  
Dna Double Strand Break ◽  
Radiation Induced ◽  
A Site

scholarly journals Regulation of Error-Prone DNA Double-Strand Break Repair and Its Impact on Genome Evolution

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1657 ◽  
Author(s):  
Terrence Hanscom ◽  
Mitch McVey
Keyword(s):  
Strand Break ◽  
Double Strand Break ◽  
Dna Lesions ◽  
Double Strand Break Repair ◽  
End Joining ◽  
Genetic Changes ◽  
Strand Breaks ◽  
Dna Double Strand Break ◽  
Alternative End Joining ◽  
Break Repair

Double-strand breaks are one of the most deleterious DNA lesions. Their repair via error-prone mechanisms can promote mutagenesis, loss of genetic information, and deregulation of the genome. These detrimental outcomes are significant drivers of human diseases, including many cancers. Mutagenic double-strand break repair also facilitates heritable genetic changes that drive organismal adaptation and evolution. In this review, we discuss the mechanisms of various error-prone DNA double-strand break repair processes and the cellular conditions that regulate them, with a focus on alternative end joining. We provide examples that illustrate how mutagenic double-strand break repair drives genome diversity and evolution. Finally, we discuss how error-prone break repair can be crucial to the induction and progression of diseases such as cancer.

scholarly journals RAD-51-Dependent and -Independent Roles of a Caenorhabditis elegans BRCA2-Related Protein during DNA Double-Strand Break Repair

2005 ◽  
Vol 25 (8) ◽  
pp. 3127-3139 ◽  
Author(s):  
Julie S. Martin ◽  
Nicole Winkelmann ◽  
Mark I. R. Petalcorin ◽  
Michael J. McIlwraith ◽  
Simon J. Boulton
Keyword(s):  
Caenorhabditis Elegans ◽  
Strand Break ◽  
Double Strand Break ◽  
Nonhomologous End Joining ◽  
Related Protein ◽  
End Joining ◽  
Dsb Repair ◽  
Phenotypic Differences ◽  
Dna Double Strand Break ◽  
Radiation Induced

ABSTRACT The BRCA2 tumor suppressor is implicated in DNA double-strand break (DSB) repair by homologous recombination (HR), where it regulates the RAD51 recombinase. We describe a BRCA2-related protein of Caenorhabditis elegans (CeBRC-2) that interacts directly with RAD-51 via a single BRC motif and that binds preferentially to single-stranded DNA through an oligonucleotide-oligosaccharide binding fold. Cebrc-2 mutants fail to repair meiotic or radiation-induced DSBs by HR due to inefficient RAD-51 nuclear localization and a failure to target RAD-51 to sites of DSBs. Genetic and cytological comparisons of Cebrc-2 and rad-51 mutants revealed fundamental phenotypic differences that suggest a role for Cebrc-2 in promoting the use of an alternative repair pathway in the absence of rad-51 and independent of nonhomologous end joining (NHEJ). Unlike rad-51 mutants, Cebrc-2 mutants also accumulate RPA-1 at DSBs, and abnormal chromosome aggregates that arise during the meiotic prophase can be rescued by blocking the NHEJ pathway. CeBRC-2 also forms foci in response to DNA damage and can do so independently of rad-51. Thus, CeBRC-2 not only regulates RAD-51 during HR but can also function independently of rad-51 in DSB repair processes.

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