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Thesis topic proposal
 
How to inactivate damaged mitochondria?

THESIS TOPIC PROPOSAL

Institute: Eötvös Loránd University, Budapest
biology
Doctoral School of Biology

Thesis supervisor: Tibor Kovács
Location of studies (in Hungarian): ELTE, TTK, Institute of Biology, Department of Genetics
Abbreviation of location of studies: ELTE


Description of the research topic:

Mitochondria are the cellular organelles that provide energy to the cell. Their shape, movement, and activity in the cell are under strict control. The damaged mitochondria are degraded through a conserved selective autophagy - mitophagy - in cells. This process involves proteins such as Pink1 or Parkin. In their absence, damaged mitochondria accumulate and release cell-damaging reactive oxygen species (ROS). Pink1 and Parkin mutations in nerve cells contribute to Parkinson's disease (predominantly due to mitophagy). This research aims to find alternative ways to reduce the levels of cytoplasmic ROS produced by damaged mitochondria in the nervous system. In the Drosophila germline, both the inactivation of mitochondria (by shape change) and their transport to the extracellular space can be studied. We aim to identify regulatory elements that can stimulate these processes in the absence of mitophagy and to investigate further their role in aging and Parkinson's disease models.

Required language skills: English
Further requirements: 
English language skills and experience in molecular biology methodology, MSc in biology.

Number of students who can be accepted: 1

Deadline for application: 2024-05-31


2024. IV. 17.
ODT ülés
Az ODT következő ülésére 2024. június 14-én, pénteken 10.00 órakor kerül sor a Semmelweis Egyetem Szenátusi termében (Bp. Üllői út 26. I. emelet).

 
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