Evidence map›Paper›PMID 21707788›Full record

ArticleMolecular microbiology2011

Role for Sit4p-dependent mitochondrial dysfunction in mediating the shortened chronological lifespan and oxidative stress sensitivity of Isc1p-deficient cells.

António Daniel Barbosa, Hugo Osório, Kellie J Sims, Teresa Almeida, Mariana Alves, Jacek Bielawski, Maria Amélia Amorim, Pedro Moradas-Ferreira, Yusuf A Hannun, Vítor Costa

Open access · bronzeAbstract read
In one paragraph

Article in Molecular microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Acetic acid induces Sch9p-dependent translocation of Isc1p from the endoplasmic reticulum into mitochondria.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Sphingolipids and lifespan regulation.Biochimica et biophysica acta · 2014
    Review
  18. Lipids and cell death in yeast.FEMS yeast research · 2014
    Review
  19. Article
  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

10 authors at 3 institutions in 2 countries.

António Daniel BarbosaIBMC, Instituto de Biologia Molecular e Celular, Grupo de Microbiologia Celular e Aplicada, Rua do Campo Alegre, 823, 4150-180 Porto, Portugal.
Hugo Osório
Kellie J Sims
Teresa Almeida
Mariana Alves
Jacek Bielawski
Maria Amélia Amorim
Pedro Moradas-Ferreira
Yusuf A Hannun
Vítor Costa
Instituto de Biologia Molecular e CelularMedical University of South Carolina · USUniversidade do Porto · PT

Funding

Sphingomyelin Turnover and Cellular RegulationR37GM043825 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI HANNUN, YUSUF AWNI · 2007 to 2015
$3.7M
Modeling and Analysis of Yeast Sphingolipid MetabolismR01GM063265 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI HANNUN, YUSUF AWNI · 2001 to 2013
$3.4M
EXTRAMURAL RESEARCH FACILITIES CONSTRUCTIONC06RR018823 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND, JOHN R · 2003 to 2003
$2.9M
SPHINGOMYELIN TURNOVER AND CELLULAR REGULATIONR01GM043825 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HANNUN, YUSUF AWNI · 1991 to 2006
$2.2M
NCRR NIH HHS C06 RR018823NIGMS NIH HHS GM43825NIGMS NIH HHS GM63265NIGMS NIH HHS R01 GM043825NIGMS NIH HHS R01 GM063265NIGMS NIH HHS R37 GM043825
6 · The paper itself

Abstract

Saccharomyces cerevisiae cells lacking Isc1p, an orthologue of mammalian neutral sphingomyelinase 2, display a shortened lifespan and an increased sensitivity to oxidative stress. A lipidomic analysis revealed specific changes in sphingolipids that accompanied the premature ageing of Isc1p-deficient cells under severe calorie restriction conditions, including a decrease of dihydrosphingosine levels and an increase of dihydro-C(26) -ceramide and phyto-C(26) -ceramide levels, the latter raising the possibility of activation of ceramide-dependent protein phosphatases. Consequently, deletion of the SIT4 gene, which encodes for the catalytic subunit of type 2A ceramide-activated protein phosphatase in yeast, abolished the premature ageing and hydrogen peroxide sensitivity of isc1Δ cells. SIT4 deletion also abolished the respiratory defects and catalase A deficiency exhibited by isc1Δ mutants. These results are consistent with catabolic derepression associated with the loss of Sit4p. The overall results show that Isc1p is an upstream regulator of Sit4p and implicate Sit4p activation in mitochondrial dysfunction leading to the shortened chronological lifespan and oxidative stress sensitivity of isc1Δ mutants.

Indexed as

Microbial ViabilityOxidative StressGene DeletionMetabolic Networks and PathwaysMitochondriaOxidantsProtein Phosphatase 2Saccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSphingolipidsType C PhospholipasesISC1 protein, S cerevisiaeOxidantsProtein Phosphatase 2Saccharomyces cerevisiae ProteinsSIT4 protein, S cerevisiaeSphingolipidsType C Phospholipases

Identifiers

PMID21707788
PMCPMC3133821
OpenAlexW2106276699

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.