The GTPase dMiro is required for axonal transport of mitochondria to Drosophila synapses.

By Xiufang Guo, G. Macleod, Andrea J. Wellington, Fangle Hu, Sarvari Panchumarthi, Miriam Schoenfield, L. Marin, M. Charlton, H. Atwood, Konrad E Zinsmaier. Neuron, 2005

628 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/712369bd2dd52e3c32bf1818b0d0028a3810bb27

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Citations in the corpus

Metabolic regulation of mitochondrial dynamics (2016, background): “The motor proteins are connected to the mitochondrial surface through receptor and adaptor proteins, whose functions were first revealed in Drosophila melanogaster neurons (Stowers et al., 2002; Guo et al., 2005).”
Mitochondrial Fusion Protects against Neurodegeneration in the Cerebellum (2007, neutral): “Genetic studies in flies suggest that neurons require abundant mitochondria at nerve termini to maintain synaptic transmission and proper ultrastructure (Guo et al., 2005; Stowers et al., 2002; Verstreken et al., 2005).”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, neutral): “By binding to both Miro (two human homologues Miro1 and Miro2) and kinesin heavy chain, Milton links mitochondria to microtubules for axonal transport (Guo et al , 2005; Glater et al , 2006).”
Negative Regulation of Active Zone Assembly by a Newly Identified SR Protein Kinase (2009, background): “In recent years, proteins have been identified that are specifically required for the anterograde transport of synaptic proteins or other cellular organelles such as mitochondria [8,17,21].”
Mitofusin 2 is necessary for transport of axonal mitochondria and interacts with the Miro/Milton complex (2010, background): “Mitochondrial transport is regulated by a series of molecular adaptors that mediate the attachment of mitochondria to molecular motors (Hollenbeck and Saxton, 2005; Kang et al., 2008; Li et al., 2009).”
Mitochondrial transport in neurons: impact on synaptic homeostasis and neurodegeneration (2012, background): “melanogaster results in impaired anterograde mitochondrial transport and the depletion of mitochondria in distal synaptic terminal”
Molecular motors in neurons: transport mechanisms and roles in brain function, development, and disease. (2010, neutral): “The Milton-Miro complex was identified as an adaptor between KIF5 and the mitochondria (Stowers et al., 2002; Fransson et al., 2003; Guo et al., 2005).”
Kinesin superfamily motor proteins and intracellular transport (2009, background): “The recent discovery of the adaptors Milton and Miro, which bridge KIF5 motors and mitochondria, has shed some light on this phenomeno”
AXONAL TRANSPORT: CARGO-SPECIFIC MECHANISMS OF MOTILITY AND REGULATION (2014, background): “The calcium-dependent arrest of mitochondrial motility is mediated by Mitochondrial Rho GTPase (Miro) (Fransson et al., 2003; Guo et al., 2005).”
Kinesin-1 and Dynein are the primary motors for fast transport of mitochondria in Drosophila motor axons. (2006, background): “More directly relevant to our study, two Drosophila proteins thought to mediate linkage of kinesin-1 to mitochondria (Milton and Miro) are required for the accumulation of mitochondria in larval axons (Stowers et al., 2002; Guo et al., 2005).”
The axonal transport of mitochondria (2005, background): “A candidate sensor, identified in a genetic screen as being necessary for mitochondrial transport to synapses (Guo et al., 2005), turned out to be the Drosophila homolog of Miro (Fransson et al., 2006), a conserved outer membrane Ca2+binding Rho-like GTPase (reviewed by Reis et al., 2009).”
Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease (2009, background): “The loss of mitochondria from axon terminals leads to synaptic dysfunction in flies (Stowers et al., 2002; Melov, 2004; Guo et al., 2005).”
Miro1 Is a Calcium Sensor for Glutamate Receptor-Dependent Localization of Mitochondria at Synapses (2009, neutral): “Trafficking of mitochondria to locations in neurons where there are large ion fluxes is essential for powering neural function.”