Csenge is a Hungarian minority of Romania who started her Biology Bsc degree at one of the best universities in Romania, Babeș-Bolyai University. After her first year of studies, she took part in a one-year Erasmus+ Exchange program in Hungary, where her studies were focused on genetics, cell- and molecular biology. This exchange year motivated her to continue an MSc program at the University of Szeged. After finishing her studies, she applied for another Erasmus+ Exchange program to start a traineeship at the University of Copenhagen, Denmark, gaining significant experience both in theoretical and practical cell biology. Eager to obtain more research skills, she is now pursuing a PhD investigating novel ciliary disease genes.

Abstract
The polycystins are two large membrane proteins that form a ciliary receptor/channel complex implicated in autosomal dominant polycystic kidney disease (PKD). In nematodes ciliary trafficking of polycystins is regulated by kinesin-3 motors, but whether this is true also in vertebrates is not clear. A recent study identified a mammalian ciliary kinesin-3 motor protein (Kif13B) that binds the scaffold protein Dlg1, localizing to cilia. Kidney-specific deletion of DLG1 in the mouse causes cilium elongation and renal cyst formation, mimicking PKD phenotypes. Furthermore, the Pedersen lab’s preliminary work in Copenhagen indicated that depletion of DLG1 or KIF13B significantly impaired polycystins’ ciliary levels but in opposite ways. The project will investigate how Dlg1/Kif13B regulates ciliary length and composition by analyzing cultures of wild type and CRISPR/Cas9-generated DLG1/KIF13B mutant kidney epithelial cells using fluorescence microscopy, live-cell imaging, and proximity labeling cilia proteomics. This will be supplemented with siRNA depletion studies, and rescue experiments will be performed using tagged versions of Dlg1/Kif13B. Ciliary cargoes of Dlg1/Kif13B will be characterized by immunoprecipitation; cell-based assays and phospho-proteomics will be used to test the effects of Dlg1/Kif13B on signaling, e.g., via PI3K/AKT and mTOR. Proteomics and data analysis will be done in collaboration with P8-EKUT and P11-CellNetworks. In collaboration with P5-OSR, test how Dlg1/Kif13B affects extracellular nutrient sensing and intracellular metabolic coordination response, as this is known to be affected in PKD.