<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sun Y</submitter><funding>NIH</funding><funding>NIH HHS</funding><funding>Kavli Institute for Brain and Mind Postdoctoral Scholar award</funding><pagination>jkaf004</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11917482</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(3)</volume><pubmed_abstract>The conserved MAP3K DLKs are widely known for their functions in synapse formation, axonal regeneration and degeneration, and neuronal survival, notably under traumatic injury and chronic disease conditions. In contrast, their roles in other neuronal compartments are much less explored. Through an unbiased forward genetic screening in C. elegans for altered patterns of GFP-tagged DLK-1 expressed from the endogenous locus, we have recently uncovered a mechanism by which the abundance of DLK-1 is tightly regulated by intraflagellar transport in ciliated sensory neurons. Here, we report additional mutants identified from the genetic screen. Most mutants exhibit increased accumulation of GFP::DLK-1 in sensory endings, and the levels of misaccumulated GFP::DLK-1 are exacerbated by loss of funct</pubmed_abstract><journal>G3 (Bethesda, Md.)</journal><pubmed_title>Multiple regulators constrain the abundance of Caenorhabditis elegans DLK-1 in ciliated sensory neurons.</pubmed_title><pmcid>PMC11917482</pmcid><funding_grant_id>NS R37 035546</funding_grant_id><funding_grant_id>NS R35 127314</funding_grant_id><funding_grant_id>P40 OD010440</funding_grant_id><pubmed_authors>Debnath A</pubmed_authors><pubmed_authors>Jin Y</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors><pubmed_authors>Zhou J</pubmed_authors><pubmed_authors>Xie B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Multiple regulators constrain the abundance of Caenorhabditis elegans DLK-1 in ciliated sensory neurons.</name><description>The conserved MAP3K DLKs are widely known for their functions in synapse formation, axonal regeneration and degeneration, and neuronal survival, notably under traumatic injury and chronic disease conditions. In contrast, their roles in other neuronal compartments are much less explored. Through an unbiased forward genetic screening in C. elegans for altered patterns of GFP-tagged DLK-1 expressed from the endogenous locus, we have recently uncovered a mechanism by which the abundance of DLK-1 is tightly regulated by intraflagellar transport in ciliated sensory neurons. Here, we report additional mutants identified from the genetic screen. Most mutants exhibit increased accumulation of GFP::DLK-1 in sensory endings, and the levels of misaccumulated GFP::DLK-1 are exacerbated by loss of funct</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Mar</publication><modification>2026-07-15T11:12:09.98Z</modification><creation>2025-04-05T22:07:23.258Z</creation></dates><accession>S-EPMC11917482</accession><cross_references><pubmed>39854273</pubmed><doi>10.1093/g3journal/jkaf004</doi></cross_references></HashMap>