Evidence map›Paper›PMID 23633144›Full record

ArticleGenetics2013

An organelle gatekeeper function for Caenorhabditis elegans UNC-16 (JIP3) at the axon initial segment.

Stacey L Edwards, Szi-chieh Yu, Christopher M Hoover, Barret C Phillips, Janet E Richmond, Kenneth G Miller

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

44 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Loss of MAPK8IP3 Affects Endocytosis in Neurons.Frontiers in cellular neuroscience · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Stacey L EdwardsGenetic Models of Disease Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA.
Szi-chieh Yu
Christopher M Hoover
Barret C Phillips
Janet E Richmond
Kenneth G Miller
Oklahoma Medical Research Foundation · USUniversity of Illinois Chicago · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
Signaling Pathways that Regulate Synaptic TransmissionR01GM080765 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MILLER, KENNETH GEORGE · 2007 to 2015
$2.7M
The role of tomosyn in synaptic transmission.R01MH073156 · NIMH · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RICHMOND, JANET E · 2006 to 2010
$2.0M
NIGMS NIH HHS GM080765NIGMS NIH HHS R01 GM080765NIH HHS P40 OD010440NIMH NIH HHS R01 MH073156
6 · The paper itself

Abstract

Neurons must cope with extreme membrane trafficking demands to produce axons with organelle compositions that differ dramatically from those of the cell soma and dendrites; however, the mechanism by which they accomplish this is not understood. Here we use electron microscopy and quantitative imaging of tagged organelles to show that Caenorhabditis elegans axons lacking UNC-16 (JIP3/Sunday Driver) accumulate Golgi, endosomes, and lysosomes at levels up to 10-fold higher than wild type, while ER membranes are largely unaffected. Time lapse microscopy of tagged lysosomes in living animals and an analysis of lysosome distributions in various regions of unc-16 mutant axons revealed that UNC-16 inhibits organelles from escaping the axon initial segment (AIS) and moving to the distal synaptic part of the axon. Immunostaining of native UNC-16 in C. elegans neurons revealed a localized concentration of UNC-16 at the initial segment, although UNC-16 is also sparsely distributed in distal regions of axons, including the synaptic region. Organelles that escape the AIS in unc-16 mutants show bidirectional active transport within the axon commissure that occasionally deposits them in the synaptic region, where their mobility decreases and they accumulate. These results argue against the long-standing, untested hypothesis that JIP3/Sunday Driver promotes anterograde organelle transport in axons and instead suggest an organelle gatekeeper model in which UNC-16 (JIP3/Sunday Driver) selectively inhibits the escape of Golgi and endosomal organelles from the AIS. This is the first evidence for an organelle gatekeeper function at the AIS, which could provide a regulatory node for controlling axon organelle composition.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAxonsBiological Transport, ActiveCaenorhabditis elegansCaenorhabditis elegans ProteinsDyneinsEndoplasmic ReticulumEndosomesGolgi ApparatusGTP-Binding Protein alpha Subunits, Gi-GoIntracellular MembranesLysosomesMitogen-Activated Protein KinasesModels, BiologicalOrganellesAdaptor Proteins, Signal TransducingCaenorhabditis elegans ProteinsDyneinsGOA-1 protein, C elegansGTP-Binding Protein alpha Subunits, Gi-GoJNK-1 protein, C elegansMitogen-Activated Protein Kinasesunc-16 protein, C elegans

Identifiers

PMID23633144
PMCPMC3632462
OpenAlexW2038232460

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.