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Regulation of NIX-mediated mitophagy by dimerization and phosphorylation (CROSBI ID 674748)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa

Marinković, Mija ; Šprung, Matilda ; Rogov, Vladimir ; Dötsch, Volker ; Dikic, Ivan ; Novak, Ivana Regulation of NIX-mediated mitophagy by dimerization and phosphorylation // Gordon Research Conference: Autophagy in Stress, Development and DIsease. 2018. str. 1-1

Podaci o odgovornosti

Marinković, Mija ; Šprung, Matilda ; Rogov, Vladimir ; Dötsch, Volker ; Dikic, Ivan ; Novak, Ivana

engleski

Regulation of NIX-mediated mitophagy by dimerization and phosphorylation

The selective removal of damaged or excess mitochondria, mitophagy, is crucial for maintaining mitochondria quality control, and globally, cellular homeostasis. Two steps are indispensable for this selective removal of mitochondria: induction of general autophagy and priming of selected mitochondria for autophagic recognition. Mitochondrial priming is mediated either by the PINK1-PARKIN signaling pathway or specific mitophagic receptors such as scAtg32, BNIP3, BCL2L13, FUNDC1, FKBP8, PHB2 and BNIP3L/NIX that interact with Atg8/LC3/GABARAP family proteins in LIR-dependent manner and recruit autophagy machinery to selected mitochondria. Previous studies have shown that autophagic receptors, in the most cases, work together in the similar selective autophagy pathway, such as aggrephagy, xenophagy and mitophagy. In the focus of our research is mitophagic receptor BNIP3L/NIX that plays a critical role in terminal differentiation of erythrocytes when complete mitochondrial content from the cell has to be removed. Our results suggest that mitophagic function of BNIP3L/NIX receptor is regulated, at least, by two possible mechanisms ; phosphorylation and homodimerization. Cellular, biochemical and biophysical evidence showed that phosphorylation of LIR domain of BNIP3L/NIX receptor enhances its interactions with Atg8/LC3/GABARAP family proteins on the autophagosomal membrane and is essential for mitophagy activation. Unfortunately we don`t know yet what is the trigger for LIR phosphorylation and activation of mitophagy. The second mechanism of BNIP3L/NIX regulation is dimerization via its transmembrane domain and our preliminary results suggest that BNIP3L/NIX homodimers recruit autophagosomes stronger than BNIP3L/NIX monomers on damaged mitochondria. Moreover, we have identified several amino acid residues in the BNIP3L/NIX transmembrane domain that are responsible for dimerization and whose substitutions lead to abolishment of the dimer formation resulting in the lower LC3/GABARAP- BNIP3L/NIX recognition and subsequently lower mitophagy induction. The latest results suggest that mitophagy initiation and progression could be achieved throught the interplay between phosphorylation and dimerization of BNIP3L/NIX receptor. Understanding of mitophagy, and general autophagy regulation, is the major challenge for researchers.

mitophagy, autophagy, NIX

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Podaci o prilogu

1-1.

2018.

nije evidentirano

objavljeno

Podaci o matičnoj publikaciji

Gordon Research Conference: Autophagy in Stress, Development and DIsease

Podaci o skupu

Gordon Research Conference: Autophagy in Stress, Development and DIsease

predavanje

17.03.2018-23.03.2018

Lucca, Italija

Povezanost rada

Biologija