ArticleThe Journal of biological chemistry2010
Cytosines, but not purines, determine recombination activating gene (RAG)-induced breaks on heteroduplex DNA structures: implications for genomic instability.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Recombination between fragile regions associated with chromosomal rearrangements in glioblastoma can be mediated by RAGs.iScience · 2025Article
- Article
- Nonamer dependent RAG cleavage at CpGs can explain mechanism of chromosomal translocations associated to lymphoid cancers.PLoS genetics · 2022Article
- Biochemical activity of RAGs is impeded by Dolutegravir, an HIV integrase inhibitor.Cell death discovery · 2020Article
- HIV integrase inhibitor, Elvitegravir, impairs RAG functions and inhibits V(D)J recombination.Cell death & disease · 2017Article
- Microhomology-mediated end joining is the principal mediator of double-strand break repair during mitochondrial DNA lesions.Molecular biology of the cell · 2016Article
- Biochemical Characterization of Nonamer Binding Domain of RAG1 Reveals its Thymine Preference with Respect to Length and Position.Scientific reports · 2016Article
- Role of recombination activating genes in the generation of antigen receptor diversity and beyond.Immunology · 2012Review
- Mechanism of fragility at BCL2 gene minor breakpoint cluster region during t(14;18) chromosomal translocation.The Journal of biological chemistry · 2012Article
- Quantitative model of R-loop forming structures reveals a novel level of RNA-DNA interactome complexity.Nucleic acids research · 2012Article
- How does DNA break during chromosomal translocations?Nucleic acids research · 2011Review
- Efficiency of nonhomologous DNA end joining varies among somatic tissues, despite similarity in mechanism.Cellular and molecular life sciences : CMLS · 2011Article
- Formation of a G-quadruplex at the BCL2 major breakpoint region of the t(14;18) translocation in follicular lymphoma.Nucleic acids research · 2011Article
- Anti-apoptotic protein BCL2 down-regulates DNA end joining in cancer cells.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sequence specificity of the recombination activating gene (RAG) complex during V(D)J recombination has been well studied. RAGs can also act as structure-specific nuclease; however, little is known about the mechanism of its action. Here, we show that in addition to DNA structure, sequence dictates the pattern and efficiency of RAG cleavage on altered DNA structures. Cytosine nucleotides are preferentially nicked by RAGs when present at single-stranded regions of heteroduplex DNA. Although unpaired thymine nucleotides are also nicked, the efficiency is many fold weaker. Induction of single- or double-strand breaks by RAGs depends on the position of cytosines and whether it is present on one or both of the strands. Interestingly, RAGs are unable to induce breaks when adenine or guanine nucleotides are present at single-strand regions. The nucleotide present immediately next to the bubble sequence could also affect RAG cleavage. Hence, we propose "C((d))C((S))C((S))" (d, double-stranded; s, single-stranded) as a consensus sequence for RAG-induced breaks at single-/double-strand DNA transitions. Such a consensus sequence motif is useful for explaining RAG cleavage on other types of DNA structures described in the literature. Therefore, the mechanism of RAG cleavage described here could explain facets of chromosomal rearrangements specific to lymphoid tissues leading to genomic instability.
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