Evidence map›Paper›PMID 33970909›Full record

ArticlePLoS biology2021

Sensitivity to expression levels underlies differential dominance of a putative null allele of the Drosophila tβh gene in behavioral phenotypes.

Christine Damrau, Julien Colomb, Björn Brembs

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 56% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Christine DamrauNeurobiologie, Institut für Biologie, Fachbereich Biologie-Chemie-Pharmazie, Freie Universität Berlin, Berlin, Germany.
Julien ColombNeurobiologie, Institut für Biologie, Fachbereich Biologie-Chemie-Pharmazie, Freie Universität Berlin, Berlin, Germany.ORCID 0000-0002-3127-5520
Björn BrembsNeurobiologie, Institut für Biologie, Fachbereich Biologie-Chemie-Pharmazie, Freie Universität Berlin, Berlin, Germany.ORCID 0000-0001-7824-7650
Freie Universität Berlin · DEUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biogenic amine octopamine (OA) and its precursor tyramine (TA) are involved in controlling a plethora of different physiological and behavioral processes. The tyramine-β-hydroxylase (tβh) gene encodes the enzyme catalyzing the last synthesis step from TA to OA. Here, we report differential dominance (from recessive to overdominant) of the putative null tβhnM18 allele in 2 behavioral measures in Buridan's paradigm (walking speed and stripe deviation) and in proboscis extension (sugar sensitivity) in the fruit fly Drosophila melanogaster. The behavioral analysis of transgenic tβh expression experiments in mutant and wild-type flies as well as of OA and TA receptor mutants revealed a complex interaction of both aminergic systems. Our analysis suggests that the different neuronal networks responsible for the 3 phenotypes show differential sensitivity to tβh gene expression levels. The evidence suggests that this sensitivity is brought about by a TA/OA opponent system modulating the involved neuronal circuits. This conclusion has important implications for standard transgenic techniques commonly used in functional genetics.

Indexed as

AllelesAnimalsAnimals, Genetically ModifiedDrosophila melanogasterDrosophila ProteinsFemaleGenotypeMaleMixed Function OxygenasesMutationOctopaminePhenotypeReceptors, Biogenic AmineTyramineDrosophila ProteinsMixed Function OxygenasesOctopamineReceptors, Biogenic AmineTyraminetyramine beta-hydroxylasetyramine receptor

Identifiers

PMID33970909
PMCPMC8136860
OpenAlexW3162806457

What OpenQuestion holds

Textmetadata
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.