Evidence map›Paper›PMID 22457822›Full record

ArticlePloS one2012

The role of the Parkinson's disease gene PARK9 in essential cellular pathways and the manganese homeostasis network in yeast.

Alessandra Chesi, Austin Kilaru, Xiaodong Fang, Antony A Cooper, Aaron D Gitler

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. ATP13A2 (PARK9) and basal ganglia function.Frontiers in neurology · 2023
    Review
  6. Article
  7. Iron-responsive-like elements and neurodegenerative ferroptosis.Learning & memory (Cold Spring Harbor, N.Y.) · 2020
    Review
  8. Cellular models of Batten disease.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Review
  9. Review
  10. Article
  11. Article
  12. Editor's Highlight: A Genome-wide Screening of Target Genes Against Silver Nanoparticles in Fission Yeast.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Article
  13. Global Deletome Profile ofFrontiers in microbiology · 2018
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

5 authors at 3 institutions in 2 countries.

Alessandra ChesiDepartment of Genetics, Stanford University School of Medicine, Stanford University, Stanford, California, United States of America.
Austin Kilaru
Xiaodong Fang
Antony A Cooper
Aaron D Gitler
University of Pennsylvania · USGarvan Institute of Medical Research · AUStanford University · US

Funding

Using yeast cells to define mechanisms of human neurodegenerative diseasesDP2OD004417 · OD · UNIVERSITY OF PENNSYLVANIA · PI GITLER, AARON D. · 2008 to 2008
$2.4M
NIH HHS 1DP2OD004417NIH HHS DP2 OD004417
6 · The paper itself

Abstract

YPK9 (Yeast PARK9; also known as YOR291W) is a non-essential yeast gene predicted by sequence to encode a transmembrane P-type transport ATPase. However, its substrate specificity is unknown. Mutations in the human homolog of YPK9, ATP13A2/PARK9, have been linked to genetic forms of early onset parkinsonism. We previously described a strong genetic interaction between Ypk9 and another Parkinson's disease (PD) protein α-synuclein in multiple model systems, and a role for Ypk9 in manganese detoxification in yeast. In humans, environmental exposure to toxic levels of manganese causes a syndrome similar to PD and is thus an environmental risk factor for the disease. How manganese contributes to neurodegeneration is poorly understood. Here we describe multiple genome-wide screens in yeast aimed at defining the cellular function of Ypk9 and the mechanisms by which it protects cells from manganese toxicity. In physiological conditions, we found that Ypk9 genetically interacts with essential genes involved in cellular trafficking and the cell cycle. Deletion of Ypk9 sensitizes yeast cells to exposure to excess manganese. Using a library of non-essential gene deletions, we screened for additional genes involved in tolerance to excess manganese exposure, discovering several novel pathways involved in manganese homeostasis. We defined the dependence of the deletion strain phenotypes in the presence of manganese on Ypk9, and found that Ypk9 deletion modifies the manganese tolerance of only a subset of strains. These results confirm a role for Ypk9 in manganese homeostasis and illuminates cellular pathways and biological processes in which Ypk9 likely functions.

Indexed as

HomeostasisGene DeletionHumansManganeseParkinson DiseaseProton-Translocating ATPasesSaccharomyces cerevisiaeATP13A2 protein, humanManganeseProton-Translocating ATPases

Identifiers

PMID22457822
PMCPMC3311584
OpenAlexW2004914033

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.