Evidence map›Paper›PMID 26306041›Full record

ArticleThe Journal of biological chemistry2015

Mitochondrial Iron-Sulfur Cluster Activity and Cytosolic Iron Regulate Iron Traffic in Saccharomyces cerevisiae.

Joshua D Wofford, Paul A Lindahl

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. A kinetic mathematical model of comprehensive iron metabolism in a respiring yeast cell: a basic-pathways approach to solving a large system dynamically.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
  2. Transcriptome Analysis and CFEM Gene Overexpression inPathogens (Basel, Switzerland) · 2025
    Article
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  12. Evidence that a respiratory shield inThe Journal of biological chemistry · 2019
    Article
  13. Contribution of Mössbauer spectroscopy to the investigation of Fe/S biogenesis.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2018
    Review
  14. Article
  15. Article
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  19. Mitochondrial iron overload: causes and consequences.Current opinion in genetics & development · 2016
    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

2 authors.

Joshua D WoffordDepartments of Chemistry, Texas A & M University, College Station, Texas 77843.
Paul A LindahlDepartments of Chemistry, Texas A & M University, College Station, Texas 77843; Departments of Chemistry, Biochemistry and Biophysics, Texas A & M University, College Station, Texas 77843. Electronic address: lindahl@chem.tamu.edu.

Funding

Iron in Mitochondrial Physiology and DiseaseR01GM084266 · NIGMS · TEXAS A&M UNIVERSITY · PI LINDAHL, PAUL A. · 2009 to 2017
$2.3M
NIGMS NIH HHS GM084266NIGMS NIH HHS R01 GM084266
6 · The paper itself

Abstract

An ordinary differential equation-based mathematical model was developed to describe trafficking and regulation of iron in growing fermenting budding yeast. Accordingly, environmental iron enters the cytosol and moves into mitochondria and vacuoles. Dilution caused by increasing cell volume is included. Four sites are regulated, including those in which iron is imported into the cytosol, mitochondria, and vacuoles, and the site at which vacuolar Fe(II) is oxidized to Fe(III). The objective of this study was to determine whether cytosolic iron (Fecyt) and/or a putative sulfur-based product of iron-sulfur cluster (ISC) activity was/were being sensed in regulation. The model assumes that the matrix of healthy mitochondria is anaerobic, and that in ISC mutants, O2 diffuses into the matrix where it reacts with nonheme high spin Fe(II) ions, oxidizing them to nanoparticles and generating reactive oxygen species. This reactivity causes a further decline in ISC/heme biosynthesis, which ultimately gives rise to the diseased state. The ordinary differential equations that define this model were numerically integrated, and concentrations of each component were plotted versus the concentration of iron in the growth medium and versus the rate of ISC/heme biosynthesis. Model parameters were optimized by fitting simulations to literature data. The model variant that assumed that both Fecyt and ISC biosynthesis activity were sensed in regulation mimicked observed behavior best. Such "dual sensing" probably arises in real cells because regulation involves assembly of an ISC on a cytosolic protein using Fecyt and a sulfur species generated in mitochondria during ISC biosynthesis and exported into the cytosol.

Indexed as

Biological Transport, ActiveComputer SimulationCytosolIronIron-Sulfur ProteinsKineticsMathematical ConceptsMetabolic Networks and PathwaysMitochondriaModels, BiologicalSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsIronIron-Sulfur ProteinsSaccharomyces cerevisiae Proteinscellular regulationFriedreich ataxiamathematical modelingmetal homeostasisMossbauer spectroscopy

Identifiers

PMID26306041
PMCPMC4646409

What OpenQuestion holds

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Registered trials

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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.