Evidence map›Paper›PMID 37267433›Full record

ArticlePLoS genetics2023

A polycistronic transgene design for combinatorial genetic perturbations from a single transcript in Drosophila.

Alexander G Teague, Maria Quintero, Fateme Karimi Dermani, Ross L Cagan, Erdem Bangi

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2023. 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 75% 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

5 authors at 1 institution in 1 country.

Alexander G TeagueDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States of America.ORCID 0000-0002-9868-3916
Maria QuinteroDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States of America.
Fateme Karimi DermaniDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States of America.
Ross L CaganDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States of America.ORCID 0000-0001-5297-450X
Erdem BangiDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States of America.ORCID 0000-0001-7390-8659
Florida State University · US

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
TRiP resources for modeling human diseaseR24OD030002 · OD · HARVARD MEDICAL SCHOOL · PI PERRIMON, NORBERT · 2020 to 2023
$3.2M
A novel Drosophila platform for sequential genetic manipulations in vivoR21GM141734 · NIGMS · FLORIDA STATE UNIVERSITY · PI BASS, HENRY W · 2021 to 2022
$424k
Modeling the genetic complexity of colorectal cancer in DrosophilaR03CA219321 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BANGI, ERDEM · 2017 to 2018
$161k
NCI NIH HHS R03 CA219321NIGMS NIH HHS R21 GM141734NIH HHS P40 OD018537NIH HHS R24 OD030002
6 · The paper itself

Abstract

Experimental models that capture the genetic complexity of human disease and allow mechanistic explorations of the underlying cell, tissue, and organ interactions are crucial to furthering our understanding of disease biology. Such models require combinatorial manipulations of multiple genes, often in more than one tissue at once. The ability to perform complex genetic manipulations in vivo is a key strength of Drosophila, where many tools for sophisticated and orthogonal genetic perturbations exist. However, combining the large number of transgenes required to establish more representative disease models and conducting mechanistic studies in these already complex genetic backgrounds is challenging. Here we present a design that pushes the limits of Drosophila genetics by allowing targeted combinatorial ectopic expression and knockdown of multiple genes from a single inducible transgene. The polycistronic transcript encoded by this transgene includes a synthetic short hairpin cluster cloned within an intron placed at the 5' end of the transcript, followed by two protein-coding sequences separated by the T2A sequence that mediates ribosome skipping. This technology is particularly useful for modeling genetically complex diseases like cancer, which typically involve concurrent activation of multiple oncogenes and loss of multiple tumor suppressors. Furthermore, consolidating multiple genetic perturbations into a single transgene further streamlines the ability to perform combinatorial genetic manipulations and makes it readily adaptable to a broad palette of transgenic systems. This flexible design for combinatorial genetic perturbations will also be a valuable tool for functionally exploring multigenic gene signatures identified from omics studies of human disease and creating humanized Drosophila models to characterize disease-associated variants in human genes. It can also be adapted for studying biological processes underlying normal tissue homeostasis and development that require simultaneous manipulation of many genes.

Indexed as

DrosophilaGenetic TechniquesAnimalsAnimals, Genetically ModifiedHumansIntronsTransgenes

Identifiers

PMID37267433
PMCPMC10266610
OpenAlexW4379184847

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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.