ArticleNucleic acids research2014
Hyperactive mariner transposons are created by mutations that disrupt allosterism and increase the rate of transposon end synapsis.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Regulatory Logic and Transposable Element Dynamics in Caenorhabditis Genomes.Genome biology and evolution · 2026Article
- Engineering of BZ transposase and transposon donor vector for enhanced efficiency and safety in gene delivery applications.Nucleic acids research · 2025Article
- Evolutionary History of the DD41D Family of Tc1/Mariner Transposons in Two Mayetiola Species.Biochemical genetics · 2025Article
- A novel hyperactive variant of theMolecular therapy. Nucleic acids · 2024Article
- Transposase expression, element abundance, element size, and DNA repair determine the mobility and heritability ofFrontiers in cell and developmental biology · 2023Article
- Progress of Transposon Vector System for Production of Recombinant Therapeutic Proteins in Mammalian Cells.Frontiers in bioengineering and biotechnology · 2022Review
- Artificial optimization of bambooFrontiers in plant science · 2022Article
- Transposon vector-mediated stable gene transfer for the accelerated establishment of recombinant mammalian cell pools allowing for high-yield production of biologics.Biotechnology letters · 2020Review
- Article
- An Engineered Cas-Transposon System for Programmable and Site-Directed DNA Transpositions.The CRISPR journal · 2019Article
- Targeted DNA transposition in vitro using a dCas9-transposase fusion protein.Nucleic acids research · 2019Article
- Host-transposon interactions: conflict, cooperation, and cooption.Genes & development · 2019Review
- Rigidity and flexibility characteristics of DD[E/D]-transposases Mos1 and Sleeping Beauty.Proteins · 2019Article
- Transposase subunit architecture and its relationship to genome size and the rate of transposition in prokaryotes and eukaryotes.Nucleic acids research · 2018Article
- Regulated complex assembly safeguards the fidelity of Sleeping Beauty transposition.Nucleic acids research · 2017Article
- Structural Determinants of Sleeping Beauty Transposase Activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Transposase interaction with the β sliding clamp: effects on insertion sequence proliferation and transposition rate.Scientific reports · 2015Article
- Structural Basis for the Inverted Repeat Preferences of mariner Transposases.The Journal of biological chemistry · 2015Article
- Structural role of the flanking DNA in mariner transposon excision.Nucleic acids research · 2015Article
- Crosstalk between transposase subunits during cleavage of the mariner transposon.Nucleic acids research · 2014Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
New applications for transposons in vertebrate genetics have spurred efforts to develop hyperactive variants. Typically, a genetic screen is used to identify several hyperactive point mutations, which are then incorporated in a single transposase gene. However, the mechanisms responsible for the increased activity are unknown. Here we show that several point mutations in the mariner transposase increase their activities by disrupting the allostery that normally serves to downregulate transposition by slowing synapsis of the transposon ends. We focused on the conserved WVPHEL amino acid motif, which forms part of the mariner transposase dimer interface. We generated almost all possible single substitutions of the W, V, E and L residues and found that the majority are hyperactive. Biochemical analysis of the mutations revealed that they disrupt signals that pass between opposite sides of the developing transpososome in response to transposon end binding. In addition to their role in allostery, the signals control the initiation of catalysis, thereby preventing non-productive double-strand breaks. Finally, we note that such breaks may explain the puzzling 'self-inflicted wounds' at the ends of the Mos1 transposon in Drosophila.
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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.