<HashMap><database>bioimages</database><scores/><additional><omics_type>Unknown</omics_type><submitter/><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-BIAD1084</full_dataset_link><repository>bioimages</repository><figure_sub>Specimen</figure_sub><figure_sub>Study Component</figure_sub><figure_sub>organisation</figure_sub><figure_sub>Biosample</figure_sub><figure_sub>Associations</figure_sub><figure_sub>Image acquisition</figure_sub><pubmed_authors>Lotte Bang Pedersen</pubmed_authors></additional><is_claimable>false</is_claimable><name>DLG1 functions upstream of SDCCAG3 and IFT20 to control ciliary targeting of polycystin-2 </name><description>Polarized vesicular trafficking directs specific receptors and ion channels to cilia, but the underlying mechanisms are poorly understood. Here we describe a role for DLG1, a core component of the Scribble polarity complex, in regulating ciliary protein trafficking in kidney epithelial cells. Conditional knockout of Dlg1 in mouse kidney caused ciliary elongation and cystogenesis, and cell-based proximity labelling proteomics and fluorescence microscopy showed alterations in the ciliary proteome upon loss of DLG1. Specifically, the retromer-associated protein SDCCAG3, IFT20 and polycystin-2 (PC2) were reduced in cilia of DLG1 deficient cells compared to control cells. This phenotype was recapitulated in vivo and rescuable by re-expression of wildtype DLG1, but not a Congenital Anomalies of </description><dates><release>2024-03-15T00:00:00Z</release><modification>2024-04-24T09:43:52.333Z</modification><creation>2024-03-15T09:26:13.97Z</creation></dates><accession>S-BIAD1084</accession><cross_references/></HashMap>