Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants

By J. C. Greene, Alexander J. Whitworth, Isabella Kuo, Laurie A. Andrews, M. Feany, L. Pallanck. Proceedings of the National Academy of Sciences of the United States of America, 2003

1,219 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Neurology

View Paper: https://www.semanticscholar.org/paper/04278c218a3286e6e38158d10dadfb0d98a53f14

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Citations in the corpus

Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control (2014, background): “We hypothesize that loss of this parkin- and PINK1-dependent trafficking mechanism impairs the ability of mitochondria to selectively degrade oxidized and damaged proteins leading, over time, to the mitochondrial dysfunction noted in PD. Keywords MDV; mitochondria; mitophagy; Parkin; PINK1 Subject…”
Role of PINK1 binding to the TOM complex and alternate intracellular membranes in recruitment and activation of the E3 ligase Parkin (2012, background): “In Drosophila, PINK1 and Parkin function in the same pathway to maintain mitochondrial fidelity (Clark et al., 2006; Greene et al., 2003; Park et al., 2006; Yang et al., 2006) supporting prior studies indicating that mitochondrial dysfunction may be a contributing factor in PD (Schapira, 2010).”
Pink1, Parkin, DJ-1 and mitochondrial dysfunction in Parkinson's disease. (2007, background): “parkin mutant flies exhibit dramatic mitochondrial defects — swollen mitochondria that have severely fragmented cristae — in several energy-intensive tissues, including the male germline and adult flight muscle [13,14].”
The Mitochondrial Basis of Aging (2016, background): “…has not been reported to exacerbate the aging phenotype of wild-type or POLG mutator mice, loss of Parkin expression in Drosophila decreases animal lifespan (Greene et al., 2003), and Parkin overexpression extends fly longevity without impairing fertility or food consumption (Rana et al., 2013).”
Mitochondrial membrane potential regulates PINK1 import and proteolytic destabilization by PARL (2010, background): “, 2006) linked to mitochondrial maintenance (Greene et al., 2003; Palacino et al., 2004; Gautier et al., 2008).”
The pathways of mitophagy for quality control and clearance of mitochondria (2012, background): “Genetic studies in Drosophila further suggested a role for PINK1 and Parkin in the regulation of mitochondrial integrity.(62,63) Loss of either protein in flies results in mitochondrial dysfunction and thereby causes degeneration of flight muscles and dopaminergic neurons.”
Human Disease Models in Drosophila melanogaster and the Role of the Fly in Therapeutic Drug Discovery (2011, background): “…melanogaster Dopaminergic neuron loss, age-dependent motor deficits, reduced lifespan, locomotor defects, male sterility and mitochondrial pathology Greene et al., 2003; Haywood and Staveley, 2004; Pesah et al., 2004; Cha et al., 2005; Sang et al., 2007 Zebrafish Dopaminergic neuron loss,…”
Drosophila orthologues to human disease genes: an update on progress. (2008, background): “Mutations in these genes lead to mitochondrial defects, muscle and locomotor dysfunction, but do not damage dopaminergic neurons (14, 15).”