Evidence map›Paper›PMID 33476638›Full record

ArticlePlasmid2021

Functional analysis of the catalytic triad of the hAT-family transposase TcBuster.

Lauren E Woodard, Felisha M Williams, Isria C Jarrett, Matthew H Wilson

Open access · greenAbstract read
In one paragraph

Article in Plasmid, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 99% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Lauren E WoodardDepartment of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN, USA; Department of Medicine, Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Biomedical Engineering, Vanderbilt University, Nashville, TN, USA. Electronic address: Lauren.Woodard@vumc.org.
Felisha M WilliamsDepartment of Medicine, Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address: Felisha.M.Williams@vumc.org.
Isria C JarrettDepartment of Medicine, Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN, USA.
Matthew H WilsonDepartment of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN, USA; Department of Medicine, Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Pharmacology, Vanderbilt University, Nashville, TN, USA. Electronic address: Matthew.Wilson@vumc.org.
Vanderbilt University Medical Center · USVanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STACIE B DUSETZINA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ALVIN C POWERS · 2012 to 2026
$29.3M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI David J. Calkins · 1989 to 2026
$19.6M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Hematology Training ProgramT32DK060445 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GOODELL, MARGARET A. · 2002 to 2023
$8.3M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
Vanderbilt O'Brien Kidney Center - Core D - Clinical and Translational CoreP30DK114809 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DE CAESTECKER, MARK P. · 2017 to 2021
$5.9M
Novel cell therapy for sustained therapeutic protein delivery in vivoR01DK093660 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, MATTHEW H · 2012 to 2022
$3.4M
Research Training in Renal DiseasesT32DK062706 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2003 to 2013
$1.5M
Kidney specific site-directed integration for cystinuriaI01BX002190 · VA · VETERANS HEALTH ADMINISTRATION · PI WILSON, MATTHEW H · 2014 to 2017
–
In Situ Reprogramming of Induced Nephron Progenitor Cells for Kidney RegenerationIK2BX002797 · VA · VETERANS HEALTH ADMINISTRATION · PI WOODARD, LAUREN ELIZABETH · 2015 to 2020
–
BLRD VA I01 BX000320BLRD VA I01 BX002190BLRD VA I01 BX004258BLRD VA I01 BX004845BLRD VA IK2 BX002797NCI NIH HHS P30 CA068485NEI NIH HHS P30 EY008126NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P30 DK058404NIDDK NIH HHS P30 DK114809NIDDK NIH HHS R01 DK093660NIDDK NIH HHS T32 DK060445NIDDK NIH HHS T32 DK062706NIDDK NIH HHS U24 DK059637NIDDK NIH HHS U2C DK059637
6 · The paper itself

Abstract

TcBuster is a hAT-family DNA transposon from the red flour beetle, Tribolium castaneum. The TcBuster transposase is of interest for genome engineering as it is highly active in insect and mammalian cells. To test the predicted catalytic triad of TcBuster, each residue of the catalytic triad of a haemagglutinin-tagged TcBuster transposase was individually mutated to a structurally conserved amino acid. Using a drug-resistant colony assay for transposon integration, we found that the D223N, D289N, and E589Q mutants of TcBuster transposase were inactive in human cells. We used a modified chromatin immunoprecipitation assay to determine that each mutant maintained binding to TcBuster transposon inverted repeat elements. Although the catalytic mutants retained their transposon binding properties, mutants displayed altered expression and localization in human cells. None of the catalytic mutants formed characteristic TcBuster transposase rodlet structures, and the D223N and D289N mutants were not able to be detected by immunofluorescence microscopy. Immunoblot analysis demonstrated that the E589Q mutant is less abundant than wild-type TcBuster transposase. Cells transfected with either TcBuster or TcBuster-E589Q transposase were imaged by structured illumination microscopy to quantify differences in the length of the transposase rodlets. The average length of the TcBuster transposase rodlets (N = 39) was 3.284 μm while the E589Q rodlets (N = 33) averaged 1.157 μm (p < 0.0001; t-test). The catalytic triad mutations decreased overall protein levels and disrupted transposase rodlet formation while nuclear localization and DNA binding to the inverted repeat elements were maintained. Our results may have broader implications for the overproduction inhibition phenomenon observed for DNA transposons.

Indexed as

DNA Transposable ElementsTransposasesAnimalsHumansMutationPlasmidsDNA Transposable ElementsTransposases(3−10): TransposonCatalytic triadhATLocalizationRodletTransposase

Identifiers

PMID33476638
PMCPMC7946762
OpenAlexW3125650111

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

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.