Evidence map›Paper›PMID 30022428›Full record

ArticleBiological trace element research2019

Iron Deficiency Reduces Synapse Formation in the Drosophila Clock Circuit.

Samuel S Rudisill, Bradley R Martin, Kevin M Mankowski, Charles R Tessier

Open access · greenAbstract read
In one paragraph

Article in Biological trace element research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Brain Iron Homeostasis and Mental Disorders.Antioxidants (Basel, Switzerland) · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Impact of Autophagy and Aging on Iron Load and Ferritin inFrontiers in cell and developmental biology · 2019
    Article
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 3 institutions in 1 country.

Samuel S RudisillDepartment of Biological Sciences, University of Notre Dame, South Bend, IN, USA.
Bradley R MartinDepartment of Biological Sciences, University of Notre Dame, South Bend, IN, USA.
Kevin M MankowskiDepartment of Medical and Molecular Genetics, Indiana University School of Medicine-South Bend, Raclin Carmichael Hall 127, 1234 Notre Dame Avenue, South Bend, IN, 46617, USA.
Charles R TessierDepartment of Medical and Molecular Genetics, Indiana University School of Medicine-South Bend, Raclin Carmichael Hall 127, 1234 Notre Dame Avenue, South Bend, IN, 46617, USA. crtessie@iu.edu.ORCID http://orcid.org/0000-0001-8931-6834
University of Notre Dame · USIndiana University School of MedicineSouth Bend Medical Foundation · US

Funding

Transition metal homeostasis in a model of Fragile X SyndromeR03MH107766 · NIMH · INDIANA UNIVERSITY INDIANAPOLIS · PI TESSIER, CHARLES R · 2016 to 2017
$157k
Indiana Clinical and Translational Sciences Institute Research Enhancement GrantNational Institute of Mental Health R03MH107766NIMH NIH HHS R03 MH107766
6 · The paper itself

Abstract

Iron serves as a critical cofactor for proteins involved in a host of biological processes. In most animals, dietary iron is absorbed in enterocytes and then disseminated for use in other tissues in the body. The brain is particularly dependent on iron. Altered iron status correlates with disorders ranging from cognitive dysfunction to disruptions in circadian activity. The exact role iron plays in producing these neurological defects, however, remains unclear. Invertebrates provide an attractive model to study the effects of iron on neuronal development since many of the genes involved in iron metabolism are conserved, and the organisms are amenable to genetic and cytological techniques. We have examined synapse growth specifically under conditions of iron deficiency in the Drosophila circadian clock circuit. We show that projections of the small ventrolateral clock neurons to the protocerebrum of the adult Drosophila brain are significantly reduced upon chelation of iron from the diet. This growth defect persists even when iron is restored to the diet. Genetic neuronal knockdown of ferritin 1 or ferritin 2, critical components of iron storage and transport, does not affect synapse growth in these cells. Together, these data indicate that dietary iron is necessary for central brain synapse formation in the fly and further validate the use of this model to study the function of iron homeostasis on brain development.

Indexed as

AnimalsBrainDrosophilaDrosophila melanogasterDrosophila ProteinsFerritinsImmunohistochemistryIron Metabolism DisordersSynapsesDrosophila ProteinsFerritinsBPSBrainChelationClockDrosophilaFerritinIronNeurodevelopmentPDFsLNvSynapse

Identifiers

PMID30022428
PMCPMC6338522
OpenAlexW2883408228

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.