Evidence map›Paper›PMID 21179194›Full record

ArticlePloS one2010

UEV-1 is an ubiquitin-conjugating enzyme variant that regulates glutamate receptor trafficking in C. elegans neurons.

Lawrence B Kramer, Jaegal Shim, Michelle L Previtera, Nora R Isack, Ming-Chih Lee, Bonnie L Firestein, Christopher Rongo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Transcriptomic Analysis ofFrontiers in psychiatry · 2019
    Article
  7. Proteasome-independent polyubiquitin linkage regulates synapse scaffolding, efficacy, and plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 2 institutions in 2 countries.

Lawrence B KramerThe Waksman Institute, Department of Genetics, Rutgers, The State University of New Jersey, Piscataway, New Jersey, United States of America.
Jaegal Shim
Michelle L Previtera
Nora R Isack
Ming-Chih Lee
Bonnie L Firestein
Christopher Rongo
Rutgers, The State University of New Jersey · USNational Cancer Center · KR

Funding

Synapse Formation in the C. elegans Nervous SystemR01NS042023 · NINDS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI RONGO, CHRISTOPHER G · 2002 to 2018
$4.6M
NINDS NIH HHS R01 NS042023NINDS NIH HHS R01 NS42023
6 · The paper itself

Abstract

The regulation of AMPA-type glutamate receptor (AMPAR) membrane trafficking is a key mechanism by which neurons regulate synaptic strength and plasticity. AMPAR trafficking is modulated through a combination of receptor phosphorylation, ubiquitination, endocytosis, and recycling, yet the factors that mediate these processes are just beginning to be uncovered. Here we identify the ubiquitin-conjugating enzyme variant UEV-1 as a regulator of AMPAR trafficking in vivo. We identified mutations in uev-1 in a genetic screen for mutants with altered trafficking of the AMPAR subunit GLR-1 in C. elegans interneurons. Loss of uev-1 activity results in the accumulation of GLR-1 in elongated accretions in neuron cell bodies and along the ventral cord neurites. Mutants also have a corresponding behavioral defect--a decrease in spontaneous reversals in locomotion--consistent with diminished GLR-1 function. The localization of other synaptic proteins in uev-1-mutant interneurons appears normal, indicating that the GLR-1 trafficking defects are not due to gross deficiencies in synapse formation or overall protein trafficking. We provide evidence that GLR-1 accumulates at RAB-10-containing endosomes in uev-1 mutants, and that receptors arrive at these endosomes independent of clathrin-mediated endocytosis. UEV-1 homologs in other species bind to the ubiquitin-conjugating enzyme Ubc13 to create K63-linked polyubiquitin chains on substrate proteins. We find that whereas UEV-1 can interact with C. elegans UBC-13, global levels of K63-linked ubiquitination throughout nematodes appear to be unaffected in uev-1 mutants, even though UEV-1 is broadly expressed in most tissues. Nevertheless, ubc-13 mutants are similar in phenotype to uev-1 mutants, suggesting that the two proteins do work together to regulate GLR-1 trafficking. Our results suggest that UEV-1 could regulate a small subset of K63-linked ubiquitination events in nematodes, at least one of which is critical in regulating GLR-1 trafficking.

Indexed as

Gene Expression RegulationAnimalsBehavior, AnimalCaenorhabditis elegansCaenorhabditis elegans ProteinsClathrinEndocytosisGenetic VariationInterneuronsModels, BiologicalModels, GeneticMutationReceptors, AMPAReceptors, GlutamateUbiquitinUbiquitin-Conjugating EnzymesCaenorhabditis elegans ProteinsClathrinReceptors, AMPAReceptors, GlutamateUbiquitinUbiquitin-Conjugating EnzymesUev-1 protein, C elegans

Identifiers

PMID21179194
PMCPMC3001443
OpenAlexW2024417855

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.