Evidence map›Paper›PMID 21988537›Full record

ArticleThe Plant journal : for cell and molecular biology2012

Accelerated cell death 2 suppresses mitochondrial oxidative bursts and modulates cell death in Arabidopsis.

Gopal K Pattanayak, Sujatha Venkataramani, Stefan Hortensteiner, Lukas Kunz, Bastien Christ, Michael Moulin, Alison G Smith, Yukihiro Okamoto, Hitoshi Tamiaki, Masakazu Sugishima and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Plant journal : for cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

25 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Oxidative stress inFrontiers in plant science · 2026
    Review
  3. Article
  4. γ-Aminobutyric Acid Alleviates Programmed Cell Death in TwoInternational journal of molecular sciences · 2024
    Article
  5. Article
  6. Singlet Oxygen Detection by Chemiluminescence Probes in Living Cells.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  7. Article
  8. Article
  9. Fine Mapping and Candidate Gene Analysis ofFrontiers in plant science · 2022
    Article
  10. Review
  11. Article
  12. Singlet Oxygen in Plants: Generation, Detection, and Signaling Roles.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. 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

11 authors at 5 institutions in 4 countries.

Gopal K PattanayakDepartment of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA.
Sujatha Venkataramani
Stefan Hortensteiner
Lukas Kunz
Bastien Christ
Michael Moulin
Alison G Smith
Yukihiro Okamoto
Hitoshi Tamiaki
Masakazu Sugishima
Jean T Greenberg
University of Chicago · USUniversity of Zurich · CHRitsumeikan University · JPUniversity of Cambridge · GBKurume University Medical Center · JP

Funding

Molecular Basis of Pathogen-Induced Cell Death in PlantsR01GM054292 · NIGMS · UNIVERSITY OF CHICAGO · PI GREENBERG, JEAN T. · 2001 to 2009
$2.6M
NIGMS NIH HHS R01 GM054292NIGMS NIH HHS R01 GM54292
6 · The paper itself

Abstract

The Arabidopsis ACCELERATED CELL DEATH 2 (ACD2) protein protects cells from programmed cell death (PCD) caused by endogenous porphyrin-related molecules like red chlorophyll catabolite or exogenous protoporphyrin IX. We previously found that during bacterial infection, ACD2, a chlorophyll breakdown enzyme, localizes to both chloroplasts and mitochondria in leaves. Additionally, acd2 cells show mitochondrial dysfunction. In plants with acd2 and ACD2 (+) sectors, ACD2 functions cell autonomously, implicating a pro-death ACD2 substrate as being cell non-autonomous in promoting the spread of PCD. ACD2 targeted solely to mitochondria can reduce the accumulation of an ACD2 substrate that originates in chloroplasts, indicating that ACD2 substrate molecules are likely to be mobile within cells. Two different light-dependent reactive oxygen bursts in mitochondria play prominent and causal roles in the acd2 PCD phenotype. Finally, ACD2 can complement acd2 when targeted to mitochondria or chloroplasts, respectively, as long as it is catalytically active: the ability to bind substrate is not sufficient for ACD2 to function in vitro or in vivo. Together, the data suggest that ACD2 localizes dynamically during infection to protect cells from pro-death mobile substrate molecules, some of which may originate in chloroplasts, but have major effects on mitochondria.

Indexed as

ApoptosisApoptosis Regulatory ProteinsArabidopsisArabidopsis ProteinsChlorophyllChloroplastsLightMitochondriaModels, BiologicalMutationOxidoreductasesPhenotypePlant LeavesReactive Oxygen SpeciesRespiratory BurstACD2 protein, ArabidopsisApoptosis Regulatory ProteinsArabidopsis ProteinsChlorophyllOxidoreductasesReactive Oxygen Species

Identifiers

PMID21988537
PMCPMC3274588
OpenAlexW2101829014

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.