Evidence map›Paper›PMID 30847993›Full record

ArticleCell proliferation2019

Lic regulates JNK-mediated cell death in Drosophila.

Yihao Sun, Di Zhang, Chenglin Li, Jiuhong Huang, Wenzhe Li, Yu Qiu, Aiwu Mao, Mingcheng Zhou, Lei Xue

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  6. Two-Faced: Roles of JNK Signalling During Tumourigenesis in theFrontiers in cell and developmental biology · 2020
    Review
  7. 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

9 authors at 3 institutions in 1 country.

Yihao SunThe First Rehabilitation Hospital of Shanghai, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0002-5829-8554
Di ZhangThe First Rehabilitation Hospital of Shanghai, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, Shanghai, China.
Chenglin LiThe First Rehabilitation Hospital of Shanghai, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, Shanghai, China.
Jiuhong HuangInternational Academy of Targeted Therapeutics and Innovation, Chongqing University of Arts and Sciences, Chongqing, China.
Wenzhe LiThe First Rehabilitation Hospital of Shanghai, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, Shanghai, China.
Yu QiuThe First Rehabilitation Hospital of Shanghai, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, Shanghai, China.
Aiwu MaoTongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Mingcheng ZhouThe First Rehabilitation Hospital of Shanghai, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, Shanghai, China.
Lei XueThe First Rehabilitation Hospital of Shanghai, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0001-6947-8414
Tongji University · CNChongqing University of Arts and Sciences · CNShanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China 31571516National Natural Science Foundation of China 31771595Shanghai Committee of Science and Technology 09DZ2260100Shanghai Committee of Science and Technology 18140900400Shanghai Committee of Science and Technology 18430711600
6 · The paper itself

Abstract

objectivesThe evolutionary conserved JNK pathway plays crucial role in cell death, yet factors that modulate this signalling have not been fully disclosed. In this study, we aim to identify additional factors that regulate JNK signalling in cell death, and characterize the underlying mechanisms. MATERIALS AND

methodsDrosophila were raised on standard media, and cross was carried out at 25°C. The Gal4/UAS system was used to express proteins or RNAi in a specific temporal and spatial pattern. Gene expression was revealed by GFP fluorescence, X-gal staining or immunostaining of 3rd instar larval eye and wing discs. Cell death was visualized by acridine orange (AO) staining. Images of fly eyes and wings were taken by OLYMPUS microscopes.

resultsWe found that licorne (lic) encoding the Drosophila MKK3 is an essential regulator of JNK-mediated cell death. Firstly, loss of lic suppressed ectopic Egr-triggered JNK activation and cell death in eye and wing development. Secondary, lic is necessary for loss-of-cell polarity-induced, physiological JNK-dependent cell death in wing development. Thirdly, Lic overexpression is sufficient to initiate JNK-mediated cell death in developing eyes and wings. Furthermore, ectopic Lic activates JNK signalling by promoting JNK phosphorylation. Finally, genetic epistatic analysis confirmed that Lic acts in parallel with Hep in the Egr-JNK pathway.

conclusionsThis study not only identified Lic as a novel component of the JNK signalling, but also disclosed the crucial roles and mechanism of Lic in cell death.

Indexed as

Cell DeathMAP Kinase Signaling SystemAnimalsAnimals, Genetically ModifiedDrosophila melanogasterDrosophila ProteinsEpistasis, GeneticEyeGene Expression Regulation, DevelopmentalGenes, InsectMembrane ProteinsMitogen-Activated Protein Kinase KinasesProtein KinasesRNA InterferenceWings, AnimalDrosophila Proteinsegr protein, DrosophilaHep protein, Drosophilalic protein, DrosophilaMembrane ProteinsMitogen-Activated Protein Kinase KinasesProtein Kinasescell deathEgrJNKLicMKK3

Identifiers

PMID30847993
PMCPMC6536442
OpenAlexW2921526781

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.