Evidence map›Paper›PMID 23870123›Full record

ArticleCell2013

Synapse location during growth depends on glia location.

Zhiyong Shao, Shigeki Watanabe, Ryan Christensen, Erik M Jorgensen, Daniel A Colón-Ramos

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Glia Development and Function in the NematodeCold Spring Harbor perspectives in biology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Molecular mechanisms of synaptogenesis.Frontiers in synaptic neuroscience · 2022
    Review
  13. Cellular basis of learning and memory in the carotid body.Frontiers in synaptic neuroscience · 2022
    Review
  14. Glia-derived temporal signals orchestrate neurogenesis in theProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Article
  16. Review
  17. Establishment and Maintenance of Neural Circuit Architecture.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Zhiyong ShaoProgram in Cellular Neuroscience, Neurodegeneration and Repair, Department of Cell Biology, Yale University School of Medicine, P.O. Box 9812, New Haven, CT 06536-0812, USA.
Shigeki Watanabe
Ryan Christensen
Erik M Jorgensen
Daniel A Colón-Ramos
Yale University · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
SYNAPTIC FUNCTION IN THE NEMATODE C. ELEGANSR01NS034307 · NINDS · UNIVERSITY OF UTAH · PI JORGENSEN, ERIK M · 1995 to 2024
$5.8M
Cellular and molecular mechanisms that temporally and spatially restrict synapticR01NS076558 · NINDS · YALE UNIVERSITY · PI COLON-RAMOS, DANIEL A · 2012 to 2022
$4.1M
Synaptic target selection in the thermotaxis neural circuit of C. elegansR00NS057931 · NINDS · YALE UNIVERSITY · PI COLON-RAMOS, DANIEL A · 2008 to 2010
$1.1M
Howard Hughes Medical InstituteNIH HHS P40 OD010440NINDS NIH HHS R00 NS057931NINDS NIH HHS R01 NS034307NINDS NIH HHS R01 NS076558
6 · The paper itself

Abstract

Synaptic contacts are largely established during embryogenesis and are then maintained during growth. To identify molecules involved in this process, we conducted a forward genetic screen in C. elegans and identified cima-1. In cima-1 mutants, synaptic contacts are correctly established during embryogenesis, but ectopic synapses emerge during postdevelopmental growth. cima-1 encodes a solute carrier in the SLC17 family of transporters that includes sialin, a protein that when mutated in humans results in neurological disorders. cima-1 does not function in neurons but rather functions in the nearby epidermal cells to correctly position glia during postlarval growth. Our findings indicate that CIMA-1 antagonizes the FGF receptor (FGFR), and does so most likely by inhibiting FGFR's role in epidermal-glia adhesion rather than signaling. Our data suggest that epidermal-glia crosstalk, in this case mediated by a transporter and the FGF receptor, is vital to preserve embryonically derived circuit architecture during postdevelopmental growth.

Indexed as

SynapsesAnimalsBody SizeCaenorhabditis elegansCaenorhabditis elegans ProteinsEmbryonic DevelopmentEpidermal CellsEpidermisMutationNeuritesNeurogliaReceptors, Fibroblast Growth FactorSodium-Phosphate Cotransporter Proteins, Type ICaenorhabditis elegans ProteinsCIMA-1 protein, C elegansEGL-15 protein, C elegansReceptors, Fibroblast Growth FactorSodium-Phosphate Cotransporter Proteins, Type I

Identifiers

PMID23870123
PMCPMC3808971
OpenAlexW2033966057

What OpenQuestion holds

Textmetadata
LicenceTDM
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.