Evidence map›Paper›PMID 31667540›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2019

Mouse model of the human serotonin transporter-linked polymorphic region.

Lukasz Piszczek, Simone Memoli, Angelo Raggioli, José Viosca, Jeanette Rientjes, Philip Hublitz, Weronika Czaban, Anna Wyrzykowska, Cornelius Gross

Open access · hybridAbstract read
In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2019. 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 86% 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, 1 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

9 authors at 5 institutions in 5 countries.

Lukasz PiszczekEpigenetics and Neurobiology Unit, European Molecular Biology Laboratory, EMBL Rome, Monterotondo, Italy. lukasz.piszczek@imp.ac.at.ORCID 0000-0003-2017-8853
Simone MemoliEpigenetics and Neurobiology Unit, European Molecular Biology Laboratory, EMBL Rome, Monterotondo, Italy.
Angelo RaggioliEpigenetics and Neurobiology Unit, European Molecular Biology Laboratory, EMBL Rome, Monterotondo, Italy.
José VioscaEpigenetics and Neurobiology Unit, European Molecular Biology Laboratory, EMBL Rome, Monterotondo, Italy.
Jeanette RientjesMonash Genome Modification Platform (MGMP), Monash University, Clayton, Australia.
Philip HublitzEpigenetics and Neurobiology Unit, European Molecular Biology Laboratory, EMBL Rome, Monterotondo, Italy.
Weronika CzabanEpigenetics and Neurobiology Unit, European Molecular Biology Laboratory, EMBL Rome, Monterotondo, Italy.
Anna WyrzykowskaEpigenetics and Neurobiology Unit, European Molecular Biology Laboratory, EMBL Rome, Monterotondo, Italy.
Cornelius GrossEpigenetics and Neurobiology Unit, European Molecular Biology Laboratory, EMBL Rome, Monterotondo, Italy. gross@embl.it.
European Molecular Biology Laboratory · ITFundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana · ESMonash University · AUResearch Institute of Molecular Pathology · ATUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic factors play a significant role in risk for mood and anxiety disorders. Polymorphisms in genes that regulate the brain monoamine systems, such as catabolic enzymes and transporters, are attractive candidates for being risk factors for emotional disorders given the weight of evidence implicating monoamines involvement in these conditions. Several common genetic variants have been identified in the human serotonin transporter (5-HTT) gene, including a repetitive sequence located in the promoter region of the locus called the serotonin transporter-linked polymorphic region (5-HTT-LPR). This polymorphism has been associated with a number of mental traits in both humans and primates, including depression, neuroticism, and harm avoidance. Some, but not all, studies found a link between the polymorphism and 5-HTT levels, leaving open the question of whether the polymorphism affects risk for mental traits via changes in 5-HTT expression. To investigate the impact of the polymorphism on gene expression, serotonin homeostasis, and behavioral traits, we set out to develop a mouse model of the human 5-HTT-LPR. Here we describe the creation and characterization of a set of mouse lines with single-copy human transgenes carrying the short and long 5-HTT-LPR variants. Although we were not able to detect differences in expression between the short and long variants, we encountered several technical issues concerning the design of our humanized mice that are likely to have influenced our findings. Our study serves as a cautionary note for future studies aimed at studying human transgene regulation in the context of the living mouse.

Indexed as

Polymorphism, GeneticAnimalsCell LineGene ExpressionHumansMice, TransgenicSerotonin Plasma Membrane Transport ProteinsTransgenesSerotonin Plasma Membrane Transport Proteins5-HTT5-HTT-LPRMouse modelsSerotonin

Identifiers

PMID31667540
PMCPMC6884432
OpenAlexW2982624991

What OpenQuestion holds

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LicenceCC BY
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.