RésuméMitochondria are complex and dynamic organelles playing many different roles in the cell such as energy production, lipid and steroid synthesis, redox signalling, regulation of calcium homeostasis and are involved in the regulation of apoptosis, immunity and inflammation. Mitochondria are an important target of choice for pathogens affecting their functions and dynamics.
In this master thesis, the link between mitochondria and Brucella abortus, an intracellular bacterial pathogen causing a zoonosis called brucellosis, has been studied. Indeed, previous studies have demonstrated that HeLa cells infected with Brucella abortus displayed mitochondrial fragmentation at 48 hours post infection, demonstrating that Brucella abortus could affect, directly or indirectly, the mitochondrial functions during the intracellular cycle/trafficking. However, the mechanisms by which mitochondrial fragmentation occurs in
infected cells and the biological consequences of this phenotype for the host cells and/or bacteria are still unknown. Therefore, we studied the functional consequences of the mitochondrial fragmentation induced by Brucella abortus.
First, we discovered that Brucella abortus induce a parkin-independent mitophagy in HeLa cells from 48 hours post infection. We next characterized the effectors involved in the mitophagy induced by Brucella abortus and found an increase in the abundance of the mitochondrial mitophagy receptor BNIP3L/NIX in infected HeLa at 48 hours post infection.
Finally, we discovered a decrease in the abundance of the external mitochondrial protein TOM20 HeLa cells infected at 72 hours post infection. Further research is still needed to fully characterize the mitophagy pathway and the function of the putative role of mitophagy for the pathogen and/or the host cells.
|la date de réponse||18 janv. 2021|
|Superviseur||Thierry Arnould (Promoteur)|