Evidence map›Paper›PMID 39774116›Full record

ArticleNature communications2025

Activity of the mammalian DNA transposon piggyBat from Myotis lucifugus is restricted by its own transposon ends.

Alison B Hickman, Laurie Lannes, Christopher M Furman, Christina Hong, Lidiya Franklin, Rodolfo Ghirlando, Arpita Ghosh, Wentian Luo, Parthena Konstantinidou, Hernán A Lorenzi and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Mining and engineering of activeSynthetic and systems biotechnology · 2027
    Article
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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

14 authors.

Alison B HickmanLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Laurie Lannes *Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Christopher M Furman *Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Christina HongLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Lidiya FranklinLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Rodolfo GhirlandoLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Arpita GhoshDepartment of Biological Sciences, Louisiana State University, Baton Rouge, LA, USA.
Wentian LuoDepartment of Medicine, Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN, USA.
Parthena KonstantinidouLaboratory of Cellular and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Hernán A LorenziLaboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-0910-7894
Anne GroveDepartment of Biological Sciences, Louisiana State University, Baton Rouge, LA, USA.ORCID http://orcid.org/0000-0002-4390-0354
Astrid D HaaseLaboratory of Cellular and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-1120-9013
Matthew H WilsonDepartment of Medicine, Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN, USA.ORCID http://orcid.org/0000-0002-3776-8350
Fred DydaLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. fred.dyda@nih.gov.ORCID http://orcid.org/0000-0003-1689-9041

Funding

Structure and function of eukaryotic DNA transposasesZIADK036153 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DYDA, FRED · 2009 to 2025
$18.9M
PIWI proteins and PIWI-interacting small RNAs guard the genomic integrity of germ cellsZIADK075111 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HAASE, ASTRID · 2015 to 2025
$14.7M
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
ChimeraX -- Next Generation Visualization and Analysis Software for Multiscale ModelingR01GM129325 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FERRIN, THOMAS E · 2018 to 2025
$5.2M
Novel cell therapy for sustained therapeutic protein delivery in vivoR01DK093660 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, MATTHEW H · 2012 to 2022
$3.4M
Next generation transposon vectors for genome engineeringR01EB033676 · NIBIB · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, MATTHEW H · 2022 to 2025
$2.0M
BLRD VA I01 BX004258Intramural NIH HHS ZIA DK036153Intramural NIH HHS ZIA DK075111National Science Foundation (NSF) MCB-2153410NIBIB NIH HHS R01 EB033676NIDDK NIH HHS P30 DK114809NIDDK NIH HHS R01 DK093660NIGMS NIH HHS R01 GM129325U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01 DK093660, R01 EB033676, P30 DK114809
6 · The paper itself

Abstract

Members of the piggyBac superfamily of DNA transposons are widely distributed in host genomes ranging from insects to mammals. The human genome has retained five piggyBac-derived genes as domesticated elements although they are no longer mobile. Here, we have investigated the transposition properties of piggyBat from Myotis lucifugus, the only known active mammalian DNA transposon, and show that its low activity in human cells is due to subterminal inhibitory DNA sequences. Activity can be dramatically improved by their removal, suggesting the existence of a mechanism for the suppression of transposon activity. The cryo-electron microscopy structure of the piggyBat transposase pre-synaptic complex showed an unexpected mode of DNA binding and recognition using C-terminal domains that are topologically different from those of the piggyBac transposase. Here we show that structure-based rational re-engineering of the transposase through the removal of putative phosphorylation sites and a changed domain organization - in combination with truncated transposon ends - results in a transposition system that is at least 100-fold more active than wild-type piggyBat.

Indexed as

ChiropteraDNA Transposable ElementsTransposasesAnimalsBinding SitesDNA FootprintingHEK293 CellsHumansPhosphorylationProtein DomainsStructure-Activity RelationshipDNA Transposable ElementsTransposases

Identifiers

PMID39774116
PMCPMC11707139

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Registered trials

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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.