<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lottes EN</submitter><funding>Georgia State University</funding><funding>NIH HHS</funding><pagination>1029</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11201622</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(12)</volume><pubmed_abstract>The development of cell-type-specific dendritic arbors is integral to the proper functioning of neurons within their circuit networks. In this study, we examine the regulatory relationship between the cytosolic chaperonin CCT, key insulin pathway genes, and an E3 ubiquitin ligase (Cullin1) in dendritic development. CCT loss of function (LOF) results in dendritic hypotrophy in &lt;i>Drosophila&lt;/i> Class IV (CIV) multi-dendritic larval sensory neurons, and CCT has recently been shown to fold components of the TOR (Target of Rapamycin) complex 1 (TORC1) in vitro. Through targeted genetic manipulations, we confirm that an LOF of CCT and the TORC1 pathway reduces dendritic complexity, while overexpression of key TORC1 pathway genes increases the dendritic complexity in CIV neurons. Furthermore, bo</pubmed_abstract><journal>Cells</journal><pubmed_title>CCT and Cullin1 Regulate the TORC1 Pathway to Promote Dendritic Arborization in Health and Disease.</pubmed_title><pmcid>PMC11201622</pmcid><funding_grant_id>GM131939</funding_grant_id><funding_grant_id>NS086082</funding_grant_id><funding_grant_id>Kenneth W. and Georganne F. Honeycutt Fellowship</funding_grant_id><funding_grant_id>2CI Neurogenomics Fellowship</funding_grant_id><funding_grant_id>NS130970</funding_grant_id><funding_grant_id>Brains &amp; Behavior Fellowship</funding_grant_id><pubmed_authors>Timmins EA</pubmed_authors><pubmed_authors>Lottes EN</pubmed_authors><pubmed_authors>Tran T</pubmed_authors><pubmed_authors>Tete B</pubmed_authors><pubmed_authors>Matta J</pubmed_authors><pubmed_authors>Cox DN</pubmed_authors><pubmed_authors>Patel AA</pubmed_authors><pubmed_authors>Ciger F</pubmed_authors><pubmed_authors>Bhattacharjee S</pubmed_authors></additional><is_claimable>false</is_claimable><name>CCT and Cullin1 Regulate the TORC1 Pathway to Promote Dendritic Arborization in Health and Disease.</name><description>The development of cell-type-specific dendritic arbors is integral to the proper functioning of neurons within their circuit networks. In this study, we examine the regulatory relationship between the cytosolic chaperonin CCT, key insulin pathway genes, and an E3 ubiquitin ligase (Cullin1) in dendritic development. CCT loss of function (LOF) results in dendritic hypotrophy in &lt;i>Drosophila&lt;/i> Class IV (CIV) multi-dendritic larval sensory neurons, and CCT has recently been shown to fold components of the TOR (Target of Rapamycin) complex 1 (TORC1) in vitro. Through targeted genetic manipulations, we confirm that an LOF of CCT and the TORC1 pathway reduces dendritic complexity, while overexpression of key TORC1 pathway genes increases the dendritic complexity in CIV neurons. Furthermore, bo</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jun</publication><modification>2025-06-01T01:39:59.077Z</modification><creation>2025-06-01T01:39:59.077Z</creation></dates><accession>S-EPMC11201622</accession><cross_references><pubmed>38920658</pubmed><doi>10.3390/cells13121029</doi></cross_references></HashMap>