Evidence map›Paper›PMID 34726300›Full record

ArticleEMBO reports2022

An exon junction complex-independent function of Barentsz in neuromuscular synapse growth.

Cheuk Hei Ho, Chiara Paolantoni, Praveen Bawankar, Zuojian Tang, Stuart Brown, Jean-Yves Roignant, Jessica E Treisman

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. 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

7 authors at 3 institutions in 3 countries.

Cheuk Hei HoSkirball Institute for Biomolecular Medicine and Department of Cell Biology, NYU School of Medicine, New York, NY, USA.
Chiara PaolantoniCenter for Integrative Genomics, Génopode Building, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Praveen BawankarInstitute of Pharmaceutical and Biomedical Sciences, Johannes Gutenberg-University Mainz, Mainz, Germany.
Zuojian TangCenter for Health Informatics and Bioinformatics, NYU Langone Medical Center, New York, NY, USA.
Stuart BrownCenter for Health Informatics and Bioinformatics, NYU Langone Medical Center, New York, NY, USA.
Jean-Yves RoignantCenter for Integrative Genomics, Génopode Building, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.ORCID 0000-0003-1395-2150
Jessica E TreismanSkirball Institute for Biomolecular Medicine and Department of Cell Biology, NYU School of Medicine, New York, NY, USA.ORCID 0000-0002-7453-107X
Johannes Gutenberg University Mainz · DENYU Langone Health · USUniversity of Lausanne · CH

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ANIRBAN MAITRA · 1985 to 2026
$83.1M
NCI NIH HHS P30 CA016087
6 · The paper itself

Abstract

The exon junction complex controls the translation, degradation, and localization of spliced mRNAs, and three of its core subunits also play a role in splicing. Here, we show that a fourth subunit, Barentsz, has distinct functions within and separate from the exon junction complex in Drosophila neuromuscular development. The distribution of mitochondria in larval muscles requires Barentsz as well as other exon junction complex subunits and is not rescued by a Barentsz transgene in which residues required for binding to the core subunit eIF4AIII are mutated. In contrast, interactions with the exon junction complex are not required for Barentsz to promote the growth of neuromuscular synapses. We find that the Activin ligand Dawdle shows reduced expression in barentsz mutants and acts downstream of Barentsz to control synapse growth. Both barentsz and dawdle are required in motor neurons, muscles, and glia for normal synapse growth, and exogenous Dawdle can rescue synapse growth in the absence of barentsz. These results identify a biological function for Barentsz that is independent of the exon junction complex.

Indexed as

Drosophila ProteinsRNA-Binding ProteinsAnimalsDrosophilaEukaryotic Initiation Factor-4AExonsSynapsesbtz protein, DrosophilaDrosophila ProteinsEukaryotic Initiation Factor-4ARNA-Binding ProteinsBarentszDawdleexon junction complexneuromuscular junctionsynapse

Identifiers

PMID34726300
PMCPMC8728599
OpenAlexW3209984740

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.