Evidence map›Paper›PMID 38581414›Full record

ArticleGenetics2024

UNC-16 interacts with LRK-1 and WDFY-3 to regulate the termination of axon growth.

Cody J Drozd, Tamjid A Chowdhury, Christopher C Quinn

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In one paragraph

Article in Genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Autism candidate genebioRxiv : the preprint server for biology · 2024
    Article
  4. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Cody J DrozdDepartment of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI 53201, USA.ORCID 0000-0002-7014-9076
Tamjid A ChowdhuryDepartment of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI 53201, USA.
Christopher C QuinnDepartment of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI 53201, USA.ORCID 0000-0002-0144-3423

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Investigation of how axon development is disrupted by the autism-causing Timothy syndrome mutation.R01MH119157 · NIMH · UNIVERSITY OF WISCONSIN MILWAUKEE · PI QUINN, CHRISTOPHER C · 2019 to 2023
$1.9M
NIH HHS P40 OD010440NIMH NIH HHS R01 MH119157NIMH NIH HHS R01MH119157
6 · The paper itself

Abstract

In humans, MAPK8IP3 (also known as JIP3) is a neurodevelopmental disorder-associated gene. In Caenorhabditis elegans, the UNC-16 ortholog of the MAPK8IP3 protein can regulate the termination of axon growth. However, its role in this process is not well understood. Here, we report that UNC-16 promotes axon termination through a process that includes the LRK-1 (LRRK-1/LRRK-2) kinase and the WDFY-3 (WDFY3/Alfy) selective autophagy protein. Genetic analysis suggests that UNC-16 promotes axon termination through an interaction between its RH1 domain and the dynein complex. Loss of unc-16 function causes accumulation of late endosomes specifically in the distal axon. Moreover, we observe synergistic interactions between loss of unc-16 function and disruptors of endolysosomal function, indicating that the endolysosomal system promotes axon termination. We also find that the axon termination defects caused by loss of UNC-16 function require the function of a genetic pathway that includes lrk-1 and wdfy-3, 2 genes that have been implicated in autophagy. These observations suggest a model where UNC-16 promotes axon termination by interacting with the endolysosomal system to regulate a pathway that includes LRK-1 and WDFY-3.

Indexed as

AxonsCaenorhabditis elegansCaenorhabditis elegans ProteinsEndosomesAdaptor Proteins, Signal TransducingAnimalsAutophagyAutophagy-Related ProteinsDyneinsNerve Tissue ProteinsProtein Serine-Threonine KinasesAdaptor Proteins, Signal TransducingAutophagy-Related ProteinsCaenorhabditis elegans ProteinsDyneinsLRK-1 protein, C elegansNerve Tissue ProteinsProtein Serine-Threonine Kinasesunc-16 protein, C elegansAlfyaxonC. elegansendosomesJIP3LRK-1LRRK2neurodevelopmentUNC-16WDFY-3

Identifiers

PMID38581414
PMCPMC11151918

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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.