Evidence map›Paper›PMID 29026112›Full record

ArticleNature communications2017

Engineering species-like barriers to sexual reproduction.

Maciej Maselko, Stephen C Heinsch, Jeremy M Chacón, William R Harcombe, Michael J Smanski

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

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  19. Gene drive and resilience through renewal with next generationProceedings of the National Academy of Sciences of the United States of America · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Maciej MaselkoDepartment of Biochemistry, Molecular Biology, and Biophysics and BioTechnology Institute, University of Minnesota - Twin Cities, Saint Paul, MN, 55108, USA.
Stephen C HeinschDepartment of Biochemistry, Molecular Biology, and Biophysics and BioTechnology Institute, University of Minnesota - Twin Cities, Saint Paul, MN, 55108, USA.ORCID http://orcid.org/0000-0003-0406-8734
Jeremy M ChacónDepartment of Ecology, Evolution, and Behavior and BioTechnology Institute, University of Minnesota - Twin Cities, Saint Paul, MN, 55108, USA.
William R HarcombeDepartment of Ecology, Evolution, and Behavior and BioTechnology Institute, University of Minnesota - Twin Cities, Saint Paul, MN, 55108, USA.
Michael J SmanskiDepartment of Biochemistry, Molecular Biology, and Biophysics and BioTechnology Institute, University of Minnesota - Twin Cities, Saint Paul, MN, 55108, USA. smanski@umn.edu.
University of Minnesota · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Controlling the exchange of genetic information between sexually reproducing populations has applications in agriculture, eradication of disease vectors, control of invasive species, and the safe study of emerging biotechnology applications. Here we introduce an approach to engineer a genetic barrier to sexual reproduction between otherwise compatible populations. Programmable transcription factors drive lethal gene expression in hybrid offspring following undesired mating events. As a proof of concept, we target the ACT1 promoter of the model organism Saccharomyces cerevisiae using a dCas9-based transcriptional activator. Lethal overexpression of actin results from mating this engineered strain with a strain containing the wild-type ACT1 promoter.Genetic isolation of a genetically modified organism represents a useful strategy for biocontainment. Here the authors use dCas9-VP64-driven gene expression to construct a 'species-like' barrier to reproduction between two otherwise compatible populations.

Indexed as

Reproductive IsolationActinsGenetic EngineeringProof of Concept StudySaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscriptional ActivationAct1 protein, S cerevisiaeActinsSaccharomyces cerevisiae Proteins

Identifiers

PMID29026112
PMCPMC5638955
OpenAlexW2950226461

What OpenQuestion holds

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LicenceCC BY
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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.