Drosophila research group 

Groupleader: Prof. Tibor Vellai


Tibor Kovács, Viktor András Billes,

Doctoral candidates (supervisor):

Manzénger, Anna (VT); Komlós, Marcell (VT); Szinyákovics, Janka (VT); Virágné, Tagscherer Kinga (BVA) 

Phd students (supervisor):

Varga, Virginia Beatrix (KT);  Radványi, Miklós (VT); Maryam, Aslam (VT); Kiss, Eszter Anna (KT); Sárközy, András Zoltán (VT),

Research field:

Autophagy is a well conserved, lysosome mediated self-degradative pathway of eukaryotic cells. Cells are able to degrade their harmful or superfluous components via autophagy, and the building blocks and energy stem from the degradation can be used for anabolic processes. In accordance, autophagy contributes to cellular homeostasis by its basal activity, which is a feature of all cells of the organisms. In addition, autophagy is able to induced by various factors. The most known such stimulus is starvation. The impairment of autophagic functions is involved in the pathomechanisms of numerous diseases. Therefore, the research of autophagy, and the better understanding of the regulation of autophagy have medical relevance as well. The most significant form of autophagy is macroautophagy. During macroautophagy, a double-membrane structure, the isolation membrane is formed which surrounds the cytoplasmic materials to be degraded. Due to the closure of the isolation membrane an autophagosome is formed, which fuses with lysosomes generating an autolysosome. The degradation takes place in the autolysosomes by the lysosomal acidic hydrolases. The fruit fly Drosophila melanogaster is one of the most widely used genetic model system which provides tools for diverse and precise genetic interventions and is highly adequate for autophagy research too. Our research group performs varied autophagy-related researches, including the examination of the role of autophagy in organ development, ageing, regeneration, organ functions, and the exploration of the more detailed molecular regulation of the autophagic processes in different organs. Our work also involves therapeutic approaches to restore autophagic activity in neurodegenerative disease models.


Relevant publications:

Manzéger A*, Tagscherer K*, Lőrincz P, Szaker H, Lukácsovich T, Pliz P, Kméczik R, Csikós G, Erdélyi M, Sass M, Kovács T, Vellai T, Billes VA: Condition-dependent functional shift of two Drosophila Mtmr lipid phosphatases in autophagy control, AUTOPHAGY 1: (19), 2021 
doi: 10.1080/15548627.2021.1899681 

Billes V*, Kovacs T*, Manzeger A, Lorincz P, Szincsak S, Regos A, Kulcsar PI, Korcsmaros T, Lukacsovich T, Hoffmann G, Erdelyi M, Mihaly J, Takacs-Vellai K, Sass M, Vellai T: Developmentally regulated autophagy is required for eye formation in Drosophila., AUTOPHAGY 14: (9) pp. 1499-1519., 2018; doi:10.1080/15548627.2018.1454569 

Kovacs T*, Billes V*, Komlos M*, Hotzi B, Manzeger A, Tarnoci A, Papp D, Szikszai F, Szinyakovics J, Racz A, Noszal B, Veszelka S, Walter FR, Deli MA, Hackler L Jr, Alfoldi R, Huzian O, Puskas LG, Liliom H, Tarnok K, Schlett K, Borsy A, Welker E, Kovacs AL, Padar Z, Erdos A, Legradi A, Bjelik A, Gulya K, Gulyas B, Vellai T: The small molecule AUTEN-99 (autophagy enhancer-99) prevents the progression of neurodegenerative symptoms., SCIENTIFIC REPORTS 7: 42014, 2017; doi:10.1038/srep42014 

Billes V*, Kovács T, Hotzi B, Manzéger A, Tagscherer K, Komlós M, Tarnóci A, Pádár Z, Erdős A, Bjelik A, Legradi A, Gulya K, Gulyás B, Vellai T: AUTEN-67 (Autophagy Enhancer-67) Hampers the Progression of Neurodegenerative Symptoms in a Drosophila model of Huntington's Disease, JOURNAL OF HUNTINGTONS DISEASE 5: (2) pp. 133-147., 2016; doi:10.3233/JHD-150180 

Papp D*, Kovacs T*, Billes V*, Varga M, Tarnoci A, Hackler L Jr, Puskas LG, Liliom H, Tarnok K, Schlett K, Borsy A, Padar Z, Kovacs AL, Hegedus K, Juhasz G, Komlos M, Erdos A, Gulyas B, Vellai T: AUTEN-67, an autophagy-enhancing drug candidate with potent antiaging and neuroprotective effects., AUTOPHAGY 12: (2) pp. 273-286., 2016; doi:10.1080/15548627.2015.1082023

*shared first author