Miro1 Regulates Mt Trafficking

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    Miro1 Regulates Activity Driven Positioning

    Mitochondria within Astrocytic Processes Appose

    Synapses to Regulate Intracellular Calcium Signaling

    Terri-Leigh Stephen et al.

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    Interaction between Presynaptic neuron and Ast

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    Role of Miro1 in mitochondria mobilty

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    Hypothesis

    Miro1 regulates trafficking and retention of mitochondria inprocesses of astrocytes and synapse.

    • This Miro1 regulated mitochondrial trafficking play a key rolintracellular calcium signaling.

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    Results

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    Fig 1: Basal

    mitochondrial

    traffickingdynamics

    differ inAstrocytic

    and Neuronal

    processes

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    Fig 2: Enhancingneuronal activity

    alters mitochondrialtrafficking dynamics

    and morphology inastrocyte processes.

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    Fig 3: Neuronal activity induces astrocyte mitochondrial posnear synapses.

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    Fig 4: Glutamatedecreases thefusion rate of

    mitochondria inastrocytic processes

    in situ.

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    Fig 5: The Calcium

    sensing EF hands

    of Miro1 areessential for

    regulatingmitochondrial

    trafficking and

    morphology inastrocytes in

    primary cultures

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    Fig 6: Mutant Miro1 expression in situ dirups the abilitmitochondria to response to neuronal activity and alte

    trafficking

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    Fig 7: Mutant Miro1 expression in slices disrupts

    intracellularastrocytes Calcium signalling

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    Pros

    • The experiments are well organized and ordered.

    •Establishes their hypothesis very well.

    • Give rise to some important questions that can lead to potefuture researches.

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    Cons

    • The mechanism by which Calcium get entry into astrocyte is not they block NMDAR mitochondrial mobility get normal, it indicateget entry through NMDA channel is responsible, but astrocytes centry involve other Glutamate dependent channels and ion exchwhy blocking them wont affect mobility.

    • They provide little emphasizes on mitochondrial fission and fusiospecially fission. It may be the proper way to answer why the

    mitochondrial length decreased.• The authors just give a reference of Miro1 dependent Mitochond

    trafficking in Neurons, but they don’t light up the mechanisms obe they can compare Neuronal and astrocytes Miro1 dependentMitochondrial trafficking in the discussion to clarify.