Evidence map›Paper›PMID 24336389›Full record

ArticleJournal of experimental botany2014

Nitric oxide induces cotyledon senescence involving co-operation of the NES1/MAD1 and EIN2-associated ORE1 signalling pathways in Arabidopsis.

Jing Du, Manli Li, Dongdong Kong, Lei Wang, Qiang Lv, Jinzheng Wang, Fang Bao, Qingqiu Gong, Jinchan Xia, Yikun He

Open access · bronzeAbstract read
In one paragraph

Article in Journal of experimental botany, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-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

15 citing papers in PubMed, 42 citations in OpenAlex.

  1. International journal of molecular sciences · 2025
    Article
  2. Article
  3. Role of Nitric Oxide in Postharvest Senescence of Fruits.International journal of molecular sciences · 2022
    Review
  4. Article
  5. Role of Nitric Oxide in Plant Senescence.Frontiers in plant science · 2022
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
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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.

Jing DuCollege of Life Sciences, Capital Normal University, Beijing, 100048, PR China.
Manli LiCollege of Life Sciences, Capital Normal University, Beijing, 100048, PR China.
Dongdong KongDepartment of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA.
Lei WangCollege of Life Sciences, Capital Normal University, Beijing, 100048, PR China.
Qiang LvCollege of Life Sciences, Capital Normal University, Beijing, 100048, PR China.
Jinzheng WangCollege of Life Sciences, Capital Normal University, Beijing, 100048, PR China.
Fang BaoCollege of Life Sciences, Capital Normal University, Beijing, 100048, PR China.
Qingqiu GongCollege of Life Sciences, Nankai University, Tianjin, 300071, PR China.
Jinchan XiaCollege of Life Sciences, Capital Normal University, Beijing, 100048, PR China.
Yikun HeCollege of Life Sciences, Capital Normal University, Beijing, 100048, PR China yhe@cnu.edu.cn.
Capital Normal University · CNNankai University · CNUniversity of Maryland, College Park · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

After germination, cotyledons undertake the major role in supplying nutrients to the pre-photoautorophy angiosperm seedlings until they senesce. Like other senescence processes, cotyledon senescence is a programmed degenerative process. Nitric oxide can induce premature cotyledon senescence in Arabidopsis thaliana, yet the underlying mechanism remains elusive. A screen for genetic mutants identified the nes1 mutant, in which cotyledon senescence was accelerated by nitric oxide. Map-based cloning revealed that NES1 is allelic to a previously reported mitotic checkpoint family gene, MAD1. The nes1/mad1 mutants were restored to the wild type, in response to nitric oxide, by transforming them with pNES1::NES1. Ectopic expression of NES1 in the wild type delayed nitric oxide-mediated cotyledon senescence, confirming the repressive role of NES1. Moreover, two positive regulators of leaf senescence, the ethylene signalling component EIN2 and the transcription factor ORE1/AtNAC2/ANAC092, were found to function during nitric oxide-induced senescence in cotyledons. The block of ORE1 function delayed senescence and ectopic expression induced the process, revealing the positive role of ORE1. EIN2 was required to induce ORE1. Furthermore, the genetic interaction analysis between NES1 and ORE1 showed that the ore1 loss-of-function mutants were epistatic to nes1, suggesting the dominant role of ORE1 and the antagonistic role of NES1 during nitric oxide-induced cotyledon senescence in Arabidopsis.

Indexed as

ArabidopsisArabidopsis ProteinsCloning, MolecularCotyledonGene Expression Regulation, PlantMutationNitric OxidePhenotypePlants, Genetically ModifiedReceptors, Cell SurfaceRepressor ProteinsSignal TransductionTranscription FactorsArabidopsis ProteinsEIN2 protein, ArabidopsisNES1 protein, ArabidopsisNitric OxideORE1 protein, ArabidopsisReceptors, Cell SurfaceRepressor ProteinsTranscription FactorsArabidopsiscotyledoninduced senescenceNES1/MAD1nitric oxideORE1/AtNAC2.

Identifiers

PMID24336389
PMCPMC4106434
OpenAlexW2158507108

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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.