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The ubiquitin signal and autophagy: an orchestrated dance leading to mitochondrial degradation
Author(s) -
Yamano Koji,
Matsuda Noriyuki,
Tanaka Keiji
Publication year - 2016
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201541486
Subject(s) - autophagy , ubiquitin , microbiology and biotechnology , degradation (telecommunications) , dance , mitochondrion , mitophagy , protein degradation , biology , chemistry , biochemistry , apoptosis , computer science , telecommunications , art , gene , literature
The quality of mitochondria, essential organelles that produce ATP and regulate numerous metabolic pathways, must be strictly monitored to maintain cell homeostasis. The loss of mitochondrial quality control systems is acknowledged as a determinant for many types of neurodegenerative diseases including Parkinson's disease ( PD ). The two gene products mutated in the autosomal recessive forms of familial early‐onset PD , Parkin and PINK 1, have been identified as essential proteins in the clearance of damaged mitochondria via an autophagic pathway termed mitophagy. Recently, significant progress has been made in understanding how the mitochondrial serine/threonine kinase PINK 1 and the E3 ligase Parkin work together through a novel stepwise cascade to identify and eliminate damaged mitochondria, a process that relies on the orchestrated crosstalk between ubiquitin/phosphorylation signaling and autophagy. In this review, we highlight our current understanding of the detailed molecular mechanisms governing Parkin‐/ PINK 1‐mediated mitophagy and the evidences connecting Parkin/ PINK 1 function and mitochondrial clearance in neurons.