Evidence map›Paper›PMID 25149397›Full record

ArticleThe Plant cell2014

Loss of ceramide kinase in Arabidopsis impairs defenses and promotes ceramide accumulation and mitochondrial H2O2 bursts.

Fang-Cheng Bi, Zhe Liu, Jian-Xin Wu, Hua Liang, Xue-Li Xi, Ce Fang, Tie-Jun Sun, Jian Yin, Guang-Yi Dai, Chan Rong and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Plant cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 108 citations in OpenAlex.

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  15. Study of Chemical Compositions and Anticancer Effects ofMolecules (Basel, Switzerland) · 2022
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  20. Metabolomics Response to Drought Stress inPlants (Basel, Switzerland) · 2021
    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

13 authors at 2 institutions in 2 countries.

Fang-Cheng BiState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Zhe LiuState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Jian-Xin WuState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Hua LiangDepartment of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, Illinois 60637.
Xue-Li XiState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Ce FangState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Tie-Jun SunState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Jian YinState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Guang-Yi DaiState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Chan RongState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Jean T GreenbergDepartment of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, Illinois 60637.
Wei-Wei SuState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.
Nan YaoState Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China yaonan@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-2045-5462
Sun Yat-sen University · CNUniversity of Chicago · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Molecular Basis of Pathogen-Induced Cell Death in PlantsR01GM054292 · NIGMS · UNIVERSITY OF CHICAGO · PI GREENBERG, JEAN T. · 2001 to 2009
$2.6M
NCATS NIH HHS UL1 TR000430NIGMS NIH HHS R01 GM054292
6 · The paper itself

Abstract

Arabidopsis thaliana plants that lack ceramide kinase, encoded by ACCELERATED CELL DEATH5 (ACD5), display spontaneous programmed cell death late in development and accumulate substrates of ACD5. Here, we compared ceramide accumulation kinetics, defense responses, ultrastructural features, and sites of reactive oxygen species (ROS) production in wild-type and acd5 plants during development and/or Botrytis cinerea infection. Quantitative sphingolipid profiling indicated that ceramide accumulation in acd5 paralleled the appearance of spontaneous cell death, and it was accompanied by autophagy and mitochondrial ROS accumulation. Plants lacking ACD5 differed significantly from the wild type in their responses to B. cinerea, showing earlier and higher increases in ceramides, greater disease, smaller cell wall appositions (papillae), reduced callose deposition and apoplastic ROS, and increased mitochondrial ROS. Together, these data show that ceramide kinase greatly affects sphingolipid metabolism and the site of ROS accumulation during development and infection, which likely explains the developmental and infection-related cell death phenotypes. The acd5 plants also showed an early defect in restricting B. cinerea germination and growth, which occurred prior to the onset of cell death. This early defect in B. cinerea restriction in acd5 points to a role for ceramide phosphate and/or the balance of ceramides in mediating early antifungal responses that are independent of cell death.

Indexed as

ApoptosisArabidopsisArabidopsis ProteinsAutophagyBotrytisCeramidesHydrogen PeroxideKineticsMitochondriaPhosphotransferases (Alcohol Group Acceptor)Reactive Oxygen SpeciesACD5 protein, ArabidopsisArabidopsis ProteinsCeramidesHydrogen PeroxidePhosphotransferases (Alcohol Group Acceptor)Reactive Oxygen Species

Identifiers

PMID25149397
PMCPMC4176443
OpenAlexW2170209421

What OpenQuestion holds

Textmetadata
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.