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.

On February 1st, 2024, she successfully defended her PhD dissertation on the Regulation of Polycystin-2 Trafficking to and at the Primary Cilium in Kidney Epithelial Cells. This research earned her a PhD degree in Biology from the University of Copenhagen.

What does Csenge do now?

After the defense, she stayed as a temporary postdoctoral fellow in the same lab, actively involved in the TheRaCil project, an EU-funded research network advancing therapies for pediatric renal ciliopathies, a group of rare genetic diseases affecting kidney function. Starting in November 2024, she will be relocating to the US to continue her postdoc in Peter Jackson’s lab at Stanford University. Her goal is to explore how specific ciliary- and non-ciliary signaling mechanisms regulate cell physiology to synergize and modulate glucose-stimulated insulin secretion (GSIS) in beta-pancreatic cells. 

What does Csenge think about our program?

I've had an amazing time during my three years as an MSCA fellow, experiencing so much personal and professional growth. I could not have asked for more of what this training program has offered and taught me over the years. It has allowed me to work in not only one but three finest institutes and to connect and collaborate with numerous peers. It is also truly remarkable to see how 14 research groups from different countries effectively communicated, whether online or in person. This has really added value and improved the quality of our research, creating a fantastic research community that we can all rely on in the future.  This experience has been invaluable for me as a PhD student. Additionally, sharing this experience with 13 other PhD students has meant I've never felt alone but instead provided endless sources of joy, unwavering support, and even lasting friendships. 

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.

We want you to understand!

Layman abstract

The polycystins are two large proteins that form a complex implicated in a disease called autosomal dominant polycystic kidney disease (AD-PKD). AD-PKD is an inherited condition affecting 1 or 2 in every 1,000 people, and for which no cure is yet available. In order to come up with a cure for AD-PKD (or any other diseases), it is crucial to understand the fundamental mechanisms and cellular processes of the polycystins. Our lab investigates how certain proteins can regulate the trafficking of polycystins within the cell.

You can also watch a 55-sec video which Csenge created to describe her research here: YOUTUBE or with others on our website here.