Evidence map›Paper›PMID 25748449›Full record

ArticlePLoS genetics2015

Drosophila S6 Kinase like inhibits neuromuscular junction growth by downregulating the BMP receptor thickveins.

Guoli Zhao, Yingga Wu, Li Du, Wenhua Li, Ying Xiong, Aiyu Yao, Qifu Wang, Yong Q Zhang

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. Glia-derived temporal signals orchestrate neurogenesis in theProceedings of the National Academy of Sciences of the United States of America · 2021
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  10. Calcium-Activated Calpain Specifically Cleaves Glutamate Receptor IIA But Not IIB at theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  11. The autophagy-related geneThe Journal of biological chemistry · 2019
    Article
  12. Article
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  14. Article
  15. Article
  16. Article
  17. Article
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  19. Review
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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

8 authors at 1 institution in 1 country.

Guoli ZhaoKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Beijing, China.
Yingga WuKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Beijing, China.
Li DuKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Beijing, China; College of Life Science, Hubei University, Wuhan, China.
Wenhua LiKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Beijing, China.
Ying XiongKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Beijing, China.
Aiyu YaoKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Beijing, China.
Qifu WangKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Beijing, China.
Yong Q ZhangKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Beijing, China.
Institute of Genetics and Developmental Biology · CN

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
NIH HHS P40 OD018537
6 · The paper itself

Abstract

Synaptic connections must be precisely controlled to ensure proper neural circuit formation. In Drosophila melanogaster, bone morphogenetic protein (BMP) promotes growth of the neuromuscular junction (NMJ) by binding and activating the BMP ligand receptors wishful thinking (Wit) and thickveins (Tkv) expressed in motor neurons. We report here that an evolutionally conserved, previously uncharacterized member of the S6 kinase (S6K) family S6K like (S6KL) acts as a negative regulator of BMP signaling. S6KL null mutants were viable and fertile but exhibited more satellite boutons, fewer and larger synaptic vesicles, larger spontaneous miniature excitatory junctional potential (mEJP) amplitudes, and reduced synaptic endocytosis at the NMJ terminals. Reducing the gene dose by half of tkv in S6KL mutant background reversed the NMJ overgrowth phenotype. The NMJ phenotypes of S6KL mutants were accompanied by an elevated level of Tkv protein and phosphorylated Mad, an effector of the BMP signaling pathway, in the nervous system. In addition, Tkv physically interacted with S6KL in cultured S2 cells. Furthermore, knockdown of S6KL enhanced Tkv expression, while S6KL overexpression downregulated Tkv in cultured S2 cells. This latter effect was blocked by the proteasome inhibitor MG132. Our results together demonstrate for the first time that S6KL regulates synaptic development and function by facilitating proteasomal degradation of the BMP receptor Tkv.

Indexed as

AnimalsAnimals, Genetically ModifiedBone Morphogenetic Protein ReceptorsBone Morphogenetic ProteinsDrosophila melanogasterDrosophila ProteinsEndocytosisMotor NeuronsNeuromuscular JunctionNeuronal PlasticityProtein Serine-Threonine KinasesProteolysisReceptors, Cell SurfaceRibosomal Protein S6 KinasesSignal TransductionSynaptic TransmissionBone Morphogenetic Protein ReceptorsBone Morphogenetic ProteinsDrosophila ProteinsProtein Serine-Threonine KinasesReceptors, Cell SurfaceRibosomal Protein S6 Kinasestkv protein, Drosophila

Identifiers

PMID25748449
PMCPMC4351882
OpenAlexW2017562733

What OpenQuestion holds

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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.