Evidence map›Paper›PMID 24319082›Full record

ArticlePlant physiology2014

The endoplasmic reticulum binding protein BiP displays dual function in modulating cell death events.

Humberto H Carvalho, Priscila A Silva, Giselle C Mendes, Otávio J B Brustolini, Maiana R Pimenta, Bianca C Gouveia, Maria Anete S Valente, Humberto J O Ramos, Juliana R L Soares-Ramos, Elizabeth P B Fontes

Open access · hybridAbstract read
In one paragraph

Article in Plant physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 10% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
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  16. Senescence-AssociatedInternational journal of molecular sciences · 2021
    Review
  17. Article
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  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 1 institution in 1 country.

Humberto H CarvalhoNational Institute of Science and Technology in Plant-Pest Interactions , Universidade Federal de Viçosa, 36570.000, Viçosa, Minas Gerais, Brazil.
Priscila A Silva
Giselle C Mendes
Otávio J B Brustolini
Maiana R Pimenta
Bianca C Gouveia
Maria Anete S Valente
Humberto J O Ramos
Juliana R L Soares-Ramos
Elizabeth P B Fontes
Universidade Federal de Viçosa · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The binding protein (BiP) has been demonstrated to participate in innate immunity and attenuate endoplasmic reticulum- and osmotic stress-induced cell death. Here, we employed transgenic plants with manipulated levels of BiP to assess whether BiP also controlled developmental and hypersensitive programmed cell death (PCD). Under normal conditions, the BiP-induced transcriptome revealed a robust down-regulation of developmental PCD genes and an up-regulation of the genes involved in hypersensitive PCD triggered by nonhost-pathogen interactions. Accordingly, the BiP-overexpressing line displayed delayed leaf senescence under normal conditions and accelerated hypersensitive response triggered by Pseudomonas syringae pv tomato in soybean (Glycine max) and tobacco (Nicotiana tabacum), as monitored by measuring hallmarks of PCD in plants. The BiP-mediated delay of leaf senescence correlated with the attenuation of N-rich protein (NRP)-mediated cell death signaling and the inhibition of the senescence-associated activation of the unfolded protein response (UPR). By contrast, under biological activation of salicylic acid (SA) signaling and hypersensitive PCD, BiP overexpression further induced NRP-mediated cell death signaling and antagonistically inhibited the UPR. Thus, the SA-mediated induction of NRP cell death signaling occurs via a pathway distinct from UPR. Our data indicate that during the hypersensitive PCD, BiP positively regulates the NRP cell death signaling through a yet undefined mechanism that is activated by SA signaling and related to ER functioning. By contrast, BiP's negative regulation of leaf senescence may be linked to its capacity to attenuate the UPR activation and NRP cell death signaling. Therefore, BiP can function either as a negative or positive modulator of PCD events.

Indexed as

Caspase 1Cell DeathEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPGene Expression ProfilingGene Expression Regulation, PlantGenes, PlantGlycine maxHeat-Shock ProteinsHost-Pathogen InteractionsModels, BiologicalPlant LeavesPlant ProteinsPlants, Genetically ModifiedProtein BindingPseudomonas syringaeCaspase 1Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsPlant Proteins

Identifiers

PMID24319082
PMCPMC3912096
OpenAlexW2168651049

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.