ArticleMolecular and cellular biology2001
RAG transposase can capture and commit to target DNA before or after donor cleavage.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Target capture during Mos1 transposition.The Journal of biological chemistry · 2014Article
- The bacterial Tn9 chloramphenicol resistance gene: an attractive DNA segment for Mos1 mariner insertions.Molecular genetics and genomics : MGG · 2009Article
- Biochemical characterization of a SET and transposase fusion protein, Metnase: its DNA binding and DNA cleavage activity.Biochemistry · 2007Article
- Target DNA structure plays a critical role in RAG transposition.PLoS biology · 2006Article
- Identification and characterization of a gain-of-function RAG-1 mutant.Molecular and cellular biology · 2006Article
- In vitro processing of the 3'-overhanging DNA in the postcleavage complex involved in V(D)J joining.Molecular and cellular biology · 2004Article
- Ordered DNA release and target capture in RAG transposition.The EMBO journal · 2004Article
- Regulation of RAG1/RAG2-mediated transposition by GTP and the C-terminal region of RAG2.The EMBO journal · 2003Article
- The C-terminal portion of RAG2 protects against transposition in vitro.The EMBO journal · 2003Article
- Inverse transposition by the RAG1 and RAG2 proteins: role reversal of donor and target DNA.The EMBO journal · 2002Article
- A RAG-1/RAG-2 tetramer supports 12/23-regulated synapsis, cleavage, and transposition of V(D)J recombination signals.Molecular and cellular biology · 2002Article
- Evidence of a critical architectural function for the RAG proteins in end processing, protection, and joining in V(D)J recombination.Genes & development · 2002Article
- Targeted transposition by the V(D)J recombinase.Molecular and cellular biology · 2002Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The discovery that the V(D)J recombinase functions as a transposase in vitro suggests that transposition by this system might be a potent source of genomic instability. To gain insight into the mechanisms that regulate transposition, we investigated a phenomenon termed target commitment that reflects a functional association between the RAG transposase and the target DNA. We found that the V(D)J recombinase is quite promiscuous, forming productive complexes with target DNA both before and after donor cleavage, and our data indicate that the rate-limiting step for transposition occurs after target capture. Formation of stable target capture complexes depends upon the presence of active-site metal binding residues (the DDE motif), suggesting that active-site amino acids in RAG-1 are critical for target capture. The ability of the RAG transposase to commit to target prior to cleavage may result in a preference for transposition into nearby targets, such as immunoglobulin and T-cell receptor loci. This could bias transposition toward relatively "safe" regions of the genome. A preference for localized transposition may also have influenced the evolution of the antigen receptor loci.
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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.