Evidence map›Paper›PMID 29373576›Full record

ArticlePLoS genetics2018

Kinesin Khc-73/KIF13B modulates retrograde BMP signaling by influencing endosomal dynamics at the Drosophila neuromuscular junction.

Edward H Liao, Lindsay Gray, Kazuya Tsurudome, Wassim El-Mounzer, Fatima Elazzouzi, Christopher Baim, Sarah Farzin, Mario R Calderon, Grant Kauwe, A Pejmun Haghighi

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. 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 23% 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, 23 citations in OpenAlex.

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  13. LDL receptor related protein 1 requires the IBiochimica et biophysica acta. Molecular cell research · 2019
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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 2 institutions in 2 countries.

Edward H LiaoBuck Institute for Research on Aging, Novato, CA, United States of America.ORCID 0000-0002-7783-1043
Lindsay GrayBuck Institute for Research on Aging, Novato, CA, United States of America.
Kazuya TsurudomeBuck Institute for Research on Aging, Novato, CA, United States of America.
Wassim El-MounzerDepartment of Physiology, McGill University, Montreal, QC, Canada.
Fatima ElazzouziDepartment of Physiology, McGill University, Montreal, QC, Canada.
Christopher BaimDepartment of Physiology, McGill University, Montreal, QC, Canada.
Sarah FarzinDepartment of Physiology, McGill University, Montreal, QC, Canada.ORCID 0000-0002-4222-6935
Mario R CalderonBuck Institute for Research on Aging, Novato, CA, United States of America.
Grant KauweBuck Institute for Research on Aging, Novato, CA, United States of America.
A Pejmun HaghighiBuck Institute for Research on Aging, Novato, CA, United States of America.ORCID 0000-0002-4928-3609
Buck Institute for Research on Aging · USMcGill University · CA

Funding

Training in Basic Research on Aging and Age-Related DiseaseT32AG000266 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Lisa M Ellerby · 1998 to 2026
$13.8M
Retrograde Regulation of Synaptic Strength by Translational MechanismsR01NS082793 · NINDS · BUCK INSTITUTE FOR RESEARCH ON AGING · PI HAGHIGHI, ALI PEJMUN · 2013 to 2022
$4.9M
NIA NIH HHS T32 AG000266NIH HHS R01NS082793NINDS NIH HHS R01 NS082793
6 · The paper itself

Abstract

Retrograde signaling is essential for neuronal growth, function and survival; however, we know little about how signaling endosomes might be directed from synaptic terminals onto retrograde axonal pathways. We have identified Khc-73, a plus-end directed microtubule motor protein, as a regulator of sorting of endosomes in Drosophila larval motor neurons. The number of synaptic boutons and the amount of neurotransmitter release at the Khc-73 mutant larval neuromuscular junction (NMJ) are normal, but we find a significant decrease in the number of presynaptic release sites. This defect in Khc-73 mutant larvae can be genetically enhanced by a partial genetic loss of Bone Morphogenic Protein (BMP) signaling or suppressed by activation of BMP signaling in motoneurons. Consistently, activation of BMP signaling that normally enhances the accumulation of phosphorylated form of BMP transcription factor Mad in the nuclei, can be suppressed by genetic removal of Khc-73. Using a number of assays including live imaging in larval motor neurons, we show that loss of Khc-73 curbs the ability of retrograde-bound endosomes to leave the synaptic area and join the retrograde axonal pathway. Our findings identify Khc-73 as a regulator of endosomal traffic at the synapse and modulator of retrograde BMP signaling in motoneurons.

Indexed as

AnimalsAnimals, Genetically ModifiedBone Morphogenetic ProteinsDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianEndosomesGene Expression Regulation, DevelopmentalKinesinsMotor NeuronsNeuromuscular JunctionPresynaptic TerminalsSignal TransductionSynapsesBone Morphogenetic ProteinsDrosophila ProteinsKhc-73 protein, DrosophilaKinesins

Identifiers

PMID29373576
PMCPMC5802963
OpenAlexW2784469065

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.