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Identifier

000417587

Title

Part I: Crosstalk between autophagy and neurotransmission. Part II: Coordination between Mitophagy and UPRmt through CHN-1/CHIP E3 ubiquitin ligase

Alternative Title

Μέρος I: Ο ρόλος της αυτοφαγίας στη νευροδιαβίβαση. Μέρος ΙΙ: Αμοιβαία σχέση μιτοφαγίας και μιτοχονδριακού UPR μέσω της Ε3 λίγασης ουβικουιτίνης CHM-1/CHIP

Author

Ασημάκη, Ευρυδίκη Κ.

Thesis advisor

Ταβερναράκης, Νεκτάριος

Reviewer

Ταλιανίδης, Ιωάννης
Ζάχος, Γεώργιος

Abstract

An essential process to maintain cellular homeostasis and functions is autophagy, a process responsible for degradation of damaged proteins and organelles. Consequently, misregulation of autophagy can result in a variety of pathological conditions. Recently, autophagy has been linked with the maintenance of meuronal homeostasis. Here, we identify important genes of autophagy like lgg-2 which is the homolog of the mammalian LC3 autophagosomal protein to play a role in synapses remodelling and neuronal exocytosis. Furthermore we link mitophagy, as well, in the process of neurotransmission, highlighting its post-synaptical function. This knowledge could prove extremely useful as synapses are critical for brain function, with synaptic dysfunction being an early pathological feature in aging and disease. In our second part of the current work we aim to investigate the crosstalk between UPR^mt and autophagy specific in mitochondria (known as mitophagy), two of the main mitochondrial quality control processes activated under pathological stress. Activation of the UPR could trigger changes in mitochondrial function or autophagy, which could modulate the UPR, exemplifying crosstalk processes. Many factors are responsible for the regulation of the magnitude , duration and function of these cellular processes. In this study we aim to investigate the role of the ubiquitin ligase CHIP in mitophagy or UPR^mt activation. We show that depletion of CHIP leads to decreased mitochondrial bioenergetics (reduced ATP levels, mitochondria membrane potential,increases PDR-1 protein levels (E3 ubiquitin-protein ligase parkin) and leads to a mild reduction in lifespan.

Language

English

Subject

Aging

C.Elegans

Lifespan

Mitochondrion

Neurotransmitters

Synapsis

Γήρανση

Μιτοχόνδριο

Νευροδιαβιβαστές