Evidence map›Paper›PMID 25393278›Full record

ArticlePLoS genetics2014

The COP9 signalosome converts temporal hormone signaling to spatial restriction on neural competence.

Yi-Chun Huang, Yu-Nung Lu, June-Tai Wu, Cheng-Ting Chien, Haiwei Pi

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 46% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Yi-Chun HuangGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan; Department of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan; Insitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
Yu-Nung LuDepartment of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan.
June-Tai WuInstitute of Molecular Biology, National Taiwan University, Taipei, Taiwan.
Cheng-Ting ChienGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan; Insitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
Haiwei PiDepartment of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan.
Chang Gung University · TWNational Defense Medical Center · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During development, neural competence is conferred and maintained by integrating spatial and temporal regulations. The Drosophila sensory bristles that detect mechanical and chemical stimulations are arranged in stereotypical positions. The anterior wing margin (AWM) is arrayed with neuron-innervated sensory bristles, while posterior wing margin (PWM) bristles are non-innervated. We found that the COP9 signalosome (CSN) suppresses the neural competence of non-innervated bristles at the PWM. In CSN mutants, PWM bristles are transformed into neuron-innervated, which is attributed to sustained expression of the neural-determining factor Senseless (Sens). The CSN suppresses Sens through repression of the ecdysone signaling target gene broad (br) that encodes the BR-Z1 transcription factor to activate sens expression. Strikingly, CSN suppression of BR-Z1 is initiated at the prepupa-to-pupa transition, leading to Sens downregulation, and termination of the neural competence of PWM bristles. The role of ecdysone signaling to repress br after the prepupa-to-pupa transition is distinct from its conventional role in activation, and requires CSN deneddylating activity and multiple cullins, the major substrates of deneddylation. Several CSN subunits physically associate with ecdysone receptors to represses br at the transcriptional level. We propose a model in which nuclear hormone receptors cooperate with the deneddylation machinery to temporally shutdown downstream target gene expression, conferring a spatial restriction on neural competence at the PWM.

Indexed as

AnimalsCOP9 Signalosome ComplexDrosophila melanogasterDrosophila ProteinsEcdysoneGene Expression Regulation, DevelopmentalMultiprotein ComplexesMutationNeuronsNuclear ProteinsPeptide HydrolasesTranscription FactorsWings, AnimalBr protein, DrosophilaCOP9 Signalosome ComplexDrosophila ProteinsEcdysoneMultiprotein ComplexesNuclear ProteinsPeptide Hydrolasessens protein, DrosophilaTranscription Factors

Identifiers

PMID25393278
PMCPMC4230841
OpenAlexW1970788691

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.