Evidence map›Paper›PMID 31175694›Full record

ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2019

Functional analysis of Aarf domain-containing kinase 1 in Drosophila melanogaster.

Dona R Wisidagama, Stefan M Thomas, Geanette Lam, Carl S Thummel

Open access · greenAbstract read
In one paragraph

Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
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

4 authors at 1 institution in 1 country.

Dona R WisidagamaDepartment of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah.
Stefan M ThomasDepartment of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah.
Geanette LamDepartment of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah.
Carl S ThummelDepartment of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah.ORCID 0000-0001-8112-4643
University of Utah · 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
Metabolic regulation of intestinal stem cell homeostasisR01CA228346 · NCI · UNIVERSITY OF UTAH · PI RUTTER, JARED P, THUMMEL, CARL S. · 2018 to 2022
$2.3M
Functions of the Mitochondrial Proteome: An Integrated Multi-Species ApproachR01GM094232 · NIGMS · UNIVERSITY OF UTAH · PI RUTTER, JARED P, THUMMEL, CARL S. · 2012 to 2015
$1.2M
NCI NIH HHS R01 CA228346NIGMS NIH HHS R01 GM094232NIH HHS P40 OD018537
6 · The paper itself

Abstract

backgroundThe ADCK proteins are predicted mitochondrial kinases. Most studies of these proteins have focused on the Abc1/Coq8 subfamily, which contributes to Coenzyme Q biosynthesis. In contrast, little is known about ADCK1 despite its evolutionary conservation in yeast, Drosophila, Caenorhabditis elegans and mammals.

resultsWe show that Drosophila ADCK1 mutants die as second instar larvae with double mouth hooks and tracheal breaks. Tissue-specific genetic rescue and RNAi studies show that ADCK1 is necessary and sufficient in the trachea for larval viability. In addition, tracheal-rescued ADCK1 mutant adults have reduced lifespan, are developmentally delayed, have reduced body size, and normal levels of basic metabolites.

conclusionThe larval lethality and double mouth hooks seen in ADCK1 mutants are often associated with reduced levels of the steroid hormone ecdysone, suggesting that this gene could contribute to controlling ecdysone levels or bioavailability. Similarly, the tracheal defects in these animals could arise from defects in intracellular lipid trafficking. These studies of ADCK1 provide a new context to define the physiological functions of this poorly understood member of the ADCK family of predicted mitochondrial proteins.

Indexed as

Abnormalities, MultipleAnimalsDrosophila melanogasterDrosophila ProteinsEcdysoneLarvaLongevityMitochondrial ProteinsMutant ProteinsProtein KinasesTracheaDrosophila ProteinsEcdysoneMitochondrial ProteinsMutant ProteinsProtein Kinasesmetabolismmitochondriamoltingtrachea

Identifiers

PMID31175694
PMCPMC7271681
OpenAlexW2970872438

What OpenQuestion holds

Textmetadata
LicenceTDM
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.