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miro-1(tm1966) mutants have ~50% wild-type mitochondrial content
"miro-1(tm1966) mutants show ~50% of wild-type mitochondrial amount"
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Reduced mitochondrial amount correlates with lifespan extension dependent on daf-16/FOXO
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Oxygen consumption only mildly reduced despite reduced mitochondrial content
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MIRO-1 physically interacts with VDAC-1
"MIRO-1 physically interacts with VDAC-1"
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Required for maintaining mitochondrial membrane potential (measured by TMRE, JC-1)
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EF-hand mutations impair membrane potential maintenance
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MIRO-1 enriched on fragmented mitochondria during stress
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MIRO-1/MTX-1/MTX-2/KLC-1 complex for kinesin-based anterograde transport
"MTX-1/2 bind MIRO-1 and kinesin light chain (KLC-1) to form adaptor complexes"
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MIRO-1/MTX-2/TRAK-1 complex for dynein-based retrograde transport
"MTX-2, MIRO-1, TRAK-1 form a distinct adaptor for dynein-based transport"
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Biochemical evidence from gel filtration and immunoprecipitation
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Genetic evidence from PVD and DA9 neuron studies
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MIRO-1 promotes RIC-7 recruitment to mitochondria
"MIRO-1 promotes recruitment/enrichment of RIC-7 on mitochondria"
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MIRO-1 optimizes but is not strictly required for anterograde transport
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miro-1 mutants show largely immobilized axonal mitochondria
"miro mutants show largely immobilized axonal mitochondria"
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Neuron-specific effects on mitochondrial distribution
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MIRO-1 required for Ca2+-dependent mitochondrial fragmentation after wounding
"Wounding triggers rapid, reversible mitochondrial fragmentation that requires MIRO-1 and cytosolic Ca2+"
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Fragmentation accelerates actin-based wound repair
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Links MIRO-1 calcium sensing to stress response
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Comprehensive review of Miro domain architecture and function
"MIRO proteins have tandem GTPase domains, tandem EF-hand Ca2+-binding motifs, and regulate motor/adaptor interactions"
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EF-hands as Ca2+ sensors regulate transport
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PINK1/Parkin targeting of Miro during mitophagy
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ER-mitochondria contact regulation